the areas i need to work on are housing footprints and good and services and cropland footprints
.
Wednesday, June 6, 2012
BOW 11
Koala
Dear mom,
Im currently endangered in Australia. i strongly miss you and all the native food. Hunters are trying to invade the home i have currently set up causing many preys to chase me. i have tried many times to hide but i feel i am running out of places. Sadly i don't eat much due that there isn't many trees here. the area is very scarce. The preys are way bigger than i am.
Being a Koala is very hard because if you don't create a home, there is no way of surviving. I'm going through rough times because the preys are taking over most of my hiding spots making me visible to the evil predators. I miss everything back home and i wish i could go pack to all my friends. Now that i am on my own, i have to be aware of all the dangers, and what food to eat and which not too.
Dear mom,
Im currently endangered in Australia. i strongly miss you and all the native food. Hunters are trying to invade the home i have currently set up causing many preys to chase me. i have tried many times to hide but i feel i am running out of places. Sadly i don't eat much due that there isn't many trees here. the area is very scarce. The preys are way bigger than i am.
Being a Koala is very hard because if you don't create a home, there is no way of surviving. I'm going through rough times because the preys are taking over most of my hiding spots making me visible to the evil predators. I miss everything back home and i wish i could go pack to all my friends. Now that i am on my own, i have to be aware of all the dangers, and what food to eat and which not too.
Thursday, March 29, 2012
Give an example of how geographic distribution can support evolution?
The fossils of a animal will be near the geography of where it died. Such as a bird fossil; if we are able to study the difference between birds now and there fossils we will be able to study changes over time and evolution. So if we find a fossil of a finch in the Galapagos islands, we can see the differences of each bird but also in whatbera they lived upon. we can figure out the type of nature they lived in before the death occured which would help us figure out its past.
Name that gene
Gene 1: Huntingtin
Huntingtin is a disease gene linked to Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons. This is thought to be caused by an expanded, unstable trinucleotide repeat in the huntingtin gene, which translates as a polyglutamine repeat in the protein product. A fairly broad range in the number of trinucleotide repeats has been identified in normal controls, and repeat numbers in excess of 40 have been described as pathological. The huntingtin locus is large, spanning 180 kb and consisting of 67 exons. The huntingtin gene is widely expressed and is required for normal development. It is expressed as 2 alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues. The larger transcript is approximately 13.7 kb and is expressed predominantly in adult and fetal brain whereas the smaller transcript of approximately 10.3 kb is more widely expressed. The genetic defect leading to Huntington's disease may not necessarily eliminate transcription, but may confer a new property on the mRNA or alter the function of the protein. One candidate is the huntingtin-associated protein-1, highly expressed in brain, which has increased affinity for huntingtin protein with expanded polyglutamine repeats. This gene contains an upstream open reading frame in the 5' UTR that inhibits expression of the huntingtin gene product through translational repression. [provided by RefSeq, Jul 2008]
Gene 2: elastin
This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Gene 3: presenilin 2 (Alzheimer disease 4)
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified. [provided by RefSeq, Jul 2008]
Gene 5: fibrillin 1
This gene encodes a member of the fibrillin family. The encoded protein is a large, extracellular matrix glycoprotein that serve as a structural component of 10-12 nm calcium-binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body. Mutations in this gene are associated with Marfan syndrome, isolated ectopia lentis, autosomal dominant Weill-Marchesani syndrome, MASS syndrome, and Shprintzen-Goldberg craniosynostosis syndrome. [provided by RefSeq, Jul 2008]
Gene 6: retino blastoma
he protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma. [provided by RefSeq, Jul 2008]
Gene 8: dystrophin
The dystrophin gene is the largest gene found in nature, measuring 2.4 Mb. The gene was identified through a positional cloning approach, targeted at the isolation of the gene responsible for Duchenne (DMD) and Becker (BMD) Muscular Dystrophies. DMD is a recessive, fatal, X-linked disorder occurring at a frequency of about 1 in 3,500 new-born males. BMD is a milder allelic form. In general, DMD patients carry mutations which cause premature translation termination (nonsense or frame shift mutations), while in BMD patients dystrophin is reduced either in molecular weight (derived from in-frame deletions) or in expression level. The dystrophin gene is highly complex, containing at least eight independent, tissue-specific promoters and two polyA-addition sites. Furthermore, dystrophin RNA is differentially spliced, producing a range of different transcripts, encoding a large set of protein isoforms. Dystrophin (as encoded by the Dp427 transcripts) is a large, rod-like cytoskeletal protein which is found at the inner surface of muscle fibers. Dystrophin is part of the dystrophin-glycoprotein complex (DGC), which bridges the inner cytoskeleton (F-actin) and the extra-cellular matrix.
Huntingtin is a disease gene linked to Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons. This is thought to be caused by an expanded, unstable trinucleotide repeat in the huntingtin gene, which translates as a polyglutamine repeat in the protein product. A fairly broad range in the number of trinucleotide repeats has been identified in normal controls, and repeat numbers in excess of 40 have been described as pathological. The huntingtin locus is large, spanning 180 kb and consisting of 67 exons. The huntingtin gene is widely expressed and is required for normal development. It is expressed as 2 alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues. The larger transcript is approximately 13.7 kb and is expressed predominantly in adult and fetal brain whereas the smaller transcript of approximately 10.3 kb is more widely expressed. The genetic defect leading to Huntington's disease may not necessarily eliminate transcription, but may confer a new property on the mRNA or alter the function of the protein. One candidate is the huntingtin-associated protein-1, highly expressed in brain, which has increased affinity for huntingtin protein with expanded polyglutamine repeats. This gene contains an upstream open reading frame in the 5' UTR that inhibits expression of the huntingtin gene product through translational repression. [provided by RefSeq, Jul 2008]
Gene 2: elastin
This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Gene 3: presenilin 2 (Alzheimer disease 4)
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified. [provided by RefSeq, Jul 2008]
Gene 5: fibrillin 1
This gene encodes a member of the fibrillin family. The encoded protein is a large, extracellular matrix glycoprotein that serve as a structural component of 10-12 nm calcium-binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body. Mutations in this gene are associated with Marfan syndrome, isolated ectopia lentis, autosomal dominant Weill-Marchesani syndrome, MASS syndrome, and Shprintzen-Goldberg craniosynostosis syndrome. [provided by RefSeq, Jul 2008]
Gene 6: retino blastoma
he protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma. [provided by RefSeq, Jul 2008]
Gene 8: dystrophin
The dystrophin gene is the largest gene found in nature, measuring 2.4 Mb. The gene was identified through a positional cloning approach, targeted at the isolation of the gene responsible for Duchenne (DMD) and Becker (BMD) Muscular Dystrophies. DMD is a recessive, fatal, X-linked disorder occurring at a frequency of about 1 in 3,500 new-born males. BMD is a milder allelic form. In general, DMD patients carry mutations which cause premature translation termination (nonsense or frame shift mutations), while in BMD patients dystrophin is reduced either in molecular weight (derived from in-frame deletions) or in expression level. The dystrophin gene is highly complex, containing at least eight independent, tissue-specific promoters and two polyA-addition sites. Furthermore, dystrophin RNA is differentially spliced, producing a range of different transcripts, encoding a large set of protein isoforms. Dystrophin (as encoded by the Dp427 transcripts) is a large, rod-like cytoskeletal protein which is found at the inner surface of muscle fibers. Dystrophin is part of the dystrophin-glycoprotein complex (DGC), which bridges the inner cytoskeleton (F-actin) and the extra-cellular matrix.
BOW 9
Predator/Prey: its an animal seized or hunted by a carnivorous animal.
Parasitism:a relation between organisms where one lives as a parasite on another.
Mutualism: relationship between two species of organisms where both benefit from the association.
Commensalism: a type of relationship between two species of a plant, animal, or fungus where one lives with, on, or in another without damage to either.
Thursday, March 15, 2012
Food Web
Producers: Fungi, Grass, Bacteria, Shrub, Tree
Primary Consumers: Squirrel, Grasshopper, Rabbit, Deer
Secondary Consumers: Shrew, Snake, Insect-eating Bird
Tertiary Consumers: Hawk and Mountain Lion
Thursday, February 16, 2012
BOW 3: Should cloning research be regulated? How, and by whom?
Tuesday, February 7, 2012
BOW 2 mutations
Non-sense mutation: Three codons tell the cell to stop providing amino acids to the protein which supposely has been reached. when this happens the process is cut short and therefore it is an incompleted process. A disease caused by this is Cystic fibrosiss.
Sense Mutation: It changes a stop in the codon into one that codes for an amino acid. The results of this event are in an elongated protein.
Deletion Mutation: when a type of gene mutation the deletion of nucleotide causes a certain shift in the reading of the codons in the mRNA.
Insertion Mutation: It results from the being of extra nucleotides in a chromosome.
Frameshift Mutation: is caused by the deletions or insertions of a number of nucleotides that is not even by a DNA sequence.
Point Mutation: It changes only asmall area or a nucleotide in a gene.
Translocation Muation:Its a mutation in which a large piece of chromosome breaks off and attaches to another chromosome.
Sense Mutation: It changes a stop in the codon into one that codes for an amino acid. The results of this event are in an elongated protein.
Deletion Mutation: when a type of gene mutation the deletion of nucleotide causes a certain shift in the reading of the codons in the mRNA.
Insertion Mutation: It results from the being of extra nucleotides in a chromosome.
Frameshift Mutation: is caused by the deletions or insertions of a number of nucleotides that is not even by a DNA sequence.
Point Mutation: It changes only asmall area or a nucleotide in a gene.
Translocation Muation:Its a mutation in which a large piece of chromosome breaks off and attaches to another chromosome.
BOW 1
Transcription: This is when the Rna copies the information of the DNA
Translation:mRNA is broken up by the ribosome to produce a amino acid or polypeptide that will later becoem into protein.
Protein Synthesis: is transcprition and translation all n one. there are many steps. The amino acids become in a sheet which then fold.
Translation:mRNA is broken up by the ribosome to produce a amino acid or polypeptide that will later becoem into protein.
Protein Synthesis: is transcprition and translation all n one. there are many steps. The amino acids become in a sheet which then fold.
Extra Credit Blog: Reflection
What topics really confused you?
I got confused on the photosynthesis and formulas. i also did not understand certain vocabulary being used. another topic i got confused on was osmosis.
What topics do you feel very clear on?
i felt clear on the Fungus topic and cells. i also felt very clear on mitosis.
What lab/ activity was your favorite? Why?
my favorite lab activity was we had to carefully pour a drop of water onto the pennies. it was my favorite because it was fun to see how many drops a penny and water could withhold.
What lab/activity was your least favorite? Why?
My least favorite lab was when we had to do the chemchi. it was my least favorite because it smelled really bad and didn't taste to great.
If you could change something about the class to make it better, for instance the type of homework (not the amount) what would it be and why?
To emphasis more on each chapter and possibly go over what we did on our homework in class.
I got confused on the photosynthesis and formulas. i also did not understand certain vocabulary being used. another topic i got confused on was osmosis.
What topics do you feel very clear on?
i felt clear on the Fungus topic and cells. i also felt very clear on mitosis.
What lab/ activity was your favorite? Why?
my favorite lab activity was we had to carefully pour a drop of water onto the pennies. it was my favorite because it was fun to see how many drops a penny and water could withhold.
What lab/activity was your least favorite? Why?
My least favorite lab was when we had to do the chemchi. it was my least favorite because it smelled really bad and didn't taste to great.
If you could change something about the class to make it better, for instance the type of homework (not the amount) what would it be and why?
To emphasis more on each chapter and possibly go over what we did on our homework in class.
Thursday, February 2, 2012
Gene Blast
Sequence 2
ATG GCG GGT CTG ACG GCG GCG GCC CCG CGG CCC GGA GTC CTC CTG CTC CTG CTG TCC ATC CTC CAC
CCC TCT CGG CCT GGA GGG GTC CCT GGG GCC ATT CCT GGT GGA GTT CCT GGA GGA GTC TT
This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Sequence 3
ATG CTC ACA TTC ATG GCC TCT GAC AGC GAG GAA GAA GTG TGT GAT GAG CGG ACG TCC CTA ATG TCG
GCC GAG AGC CCC AGC CCG CGC TCC TGC CAG GAG GGC AGG CAG GGC CCA GAG GAT GGA G
Summary: Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified. [provided by RefSeq, Jul 2008]
Sequence 6
ATG CCG CCC AAA ACC CCC CGA AAA ACG GCC GCC ACC GCC GCC GCT GCC GCC GCG GAA CCC GGC ACC
GCC GCC GCC GCC CCC TCC TGA GGG ACC CAG AGC AGG ACA GCG GCC CGG AGG AC
Summary: The protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma. [provided by RefSeq, Jul 2008]
Sequence 8
ATG CCA TCT TCC TTG ATG TTG GAG GTA CCT GCT CTG GCA GAT TTC AAC CGG GCT TGG ACA GAA
CTT ACC GAC TGG CTT TCT CTG CTT GAT CAA GTT ATA AAA TCA CAG AGG GTG ATG GTG GGT GAC CTT
Summary: The dystrophin gene is the largest gene found in nature, measuring 2.4 Mb. The gene was identified through a positional cloning approach, targeted at the isolation of the gene responsible for Duchenne (DMD) and Becker (BMD) Muscular Dystrophies. DMD is a recessive, fatal, X-linked disorder occurring at a frequency of about 1 in 3,500 new-born males. BMD is a milder allelic form. In general, DMD patients carry mutations which cause premature translation termination (nonsense or frame shift mutations), while in BMD patients dystrophin is reduced either in molecular weight (derived from in-frame deletions) or in expression level. The dystrophin gene is highly complex, containing at least eight independent, tissue-specific promoters and two polyA-addition sites. Furthermore, dystrophin RNA is differentially spliced, producing a range of different transcripts, encoding a large set of protein isoforms. Dystrophin (as encoded by the Dp427 transcripts) is a large, rod-like cytoskeletal protein which is found at the inner surface of muscle fibers. Dystrophin is part of the dystrophin-glycoprotein complex (DGC), which bridges the inner cytoskeleton (F-actin) and the extra-cellular matrix. [provided by RefSeq, Jul 2008]
Saturday, January 21, 2012
What has surprised or fascinated you from the Hot Zone so far?
the events that have surprised me the most is how quickly a disease can spread. A lot of people can be put in danger with a simple mistake. it is ridiculous can many these scientists in the book have made many dangerous mistakes that caused the deaths of their patients. it is incredible how the first patient didn't bother to warn anyone that he was sick. but even worse, he did not consider what lives he would be putting in danger on the plane.
Blog 7 How does a vaccination stop a virus?
Vaccination is the process done by injecting a dose of weak virus into your body to help the body with the disease. The immune system will be strong enough to fight off a dose of the virus so when the actual disease hits, your body is immune to it. With the vaccination the body will not be affected majorly by the disease.
Blog 4 Microscope Comparison
blog 5 three types of cells
a cell that transmits information by chemical signaling
Blog 10 Describe some positive benefits of fungi
There are many positive benefits of fungi. For example, in nature they are decomposers. Fungi is used in food production.A one type of fungi is yeast. Yeast can be used in bread and beer. There are about 200 different types of mushrooms that are edible which are Fungi.
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