Essay Available:
Pages:
3 pages/≈825 words
Sources:
4 Sources
Style:
MLA
Subject:
Health, Medicine, Nursing
Type:
Research Paper
Language:
English (U.S.)
Document:
MS Word
Date:
Total cost:
$ 17.5
Topic:
Parkinson's Disease BIO360HONG_2011SpV1.2
Research Paper Instructions:
BIO360HONG_2011SpV1.2.pdf
Writing assignment (50 pts)
Recent advances for rare genetic disease/disorder in humans or genetically
engineered plants or animals for commercial use
(No Down Syndrome, Sickle cell disease, cyctic fibrosis, or Huntington disease allowed;
No model organisms allowed: C. elegans, Drosophila, Arabidopsis, mice, etc.)
To find human genetic conditions, you can use The National Library of Medicineʼs
Genetic Home Reference (http://ghr(dot)nlm(dot)nih(dot)gov/BrowseConditions). Note that this is not
a professional level source and the information it provides is not referenced to original
sources, so you may not use it as a source for your paper and you may not cite it.
A 3-page double-spaced summary of a literature search describing IN YOUR OWN
WORDS (no quotations allowed) what has been recently (within the last 3 years: 2008-
present) discovered about your chosen genetic disease/disorder. You will need to
include at least 3 primary sources (original research data) and as many secondary
sources as you like (review articles, NO WEBSITES or BOOKS ALLOWED) for a total of
at least 4 resources.
COPYING ANY SENTENCE OR PHRASE WITHOUT QUOTATIONS IS PLAGIARISM
AND WILL BE PROSECUTED. All sentences must be in text cited and there are no
quotes allowed. All must be in your own words (Changing or leaving out one word in
a sentence or rearranging phrases in a sentence is NOT OK). For information about
what is plagiarism and what is not, see this extremely helpful website
http://www(dot)bio(dot)davidson(dot)edu/dept/plagiarism.html. Below is a direct quotation from this
site.
“Direct quotations- Let's start with the obvious. If you repeat someone else's words
verbatim, you must enclose those words in quotation marks and provide a citation. For
the citation to be complete, there MUST be a properly formatted in-text citation at the
end of the sentence and a corresponding entry in your list of references (see section
below on how to cite sources). It is not sufficient simply to name the source within the
sentence. Omitting quotation marks and/or a complete citation is considered plagiarism.
Keep in mind that direct quotations are not commonly used in scientific writings such as
lab reports or grant proposals but can be appropriate in biology essays and term papers.
Make sure that any direct quotations flow smoothly within your own thought progression
in the assignment; your task is to synthesize the relevant literature, not just copy and
paste direct quotes from each source or provide a summary sentence for each.
Paraphrasing- Paraphrasing is restating someone else's ideas while not copying
verbatim. There are acceptable and unacceptable ways to paraphrase, and it is crucial
that you understand the difference. Unacceptable paraphrasing includes any of the
following: 1) using phrases from the original source without enclosing them in quotation
marks; 2) emulating sentence structure even when using different wording; 3) emulating
paragraph organization even when using different wording or sentence structure.
Unacceptable paraphrasing--even with correct citation--is considered plagiarism.
When you do paraphrase in an acceptable manner, a proper citation is always required.
Omitting a citation is considered plagiarism.”
http://www(dot)bio(dot)davidson(dot)edu/dept/plagiarism.html
The paper will include in YOUR OWN WORDS:
BIO360 (Hong)
6
a. A short one paragraph general introduction describing your topic.
b. Description of disease or genetically modified organism using at least 3 recent
(2008-present) experiments that have been performed in the laboratory from
primary sources. (No Case Studies, Cohort Studies, or epidemiology allowed). State
the specific DNA  protein  phenotype changes. You should include the purpose,
the hypothesis, experimental design, the results, and conclusions IN YOUR OWN
WORDS. (i.e. What was the purpose, What was the hypothesis, what did the study
do, how did they do it, what did they find, and what did it mean?)
c. In-text citations using one of the styles in your primary research article (name the
journal style next to your References heading; e.g. Nature, Science, Genetics).
d. Typed reference list at the end of the paper using one of the styles in your primary
research article (in addition to the 3 pages). You must include at least 3 primary
sources, no webpages, no books, and at least 4 total. The rest can be secondary
sources (review articles are appropriate secondary sources).
Please use the PubMed internet search engine for finding articles. If you are new
to PubMed, you can learn to use it by trial and error, or use the PubMed
Tutorial (http://www(dot)nlm(dot)nih(dot)gov/bsd/disted/pubmedtutorial/).
Do not cite any source that ends in .com, .org, .net etc. These are dynamic web
pages, not references.
Do not cite the search engine you used.
For additional information or help, please use the CSUN Library or Library
resources at http://library(dot)csun(dot)edu and the CSUN Learning Resource Center
and Writing Lab at http://www(dot)csun(dot)edu/lrc/
e. Neatly typed with one inch margins, double-spaced, 12 point ARIAL font, and 3
pages max (not including References section). Sections: Introduction (hypothesis?
Expectation); Methods; Results (observation?); Discussion; References.
Grading rubric
Followed directions (appropriate topic, sources, page limit, etc) 10 points
Original writing (no plagiarism, intended or unintended) 10 points
Molecular description (how does the genotype affect the phenotype) 10 points
Methodology (3 independent experiments or findings) 10 points
Citations (use one style, state the journal style) 5 points
Mechanics (spelling; grammar; sentence structure) 5 points
You will have the opportunity to check your turnitin.com “similarity report“ before turning
in your version for my plagiarism analysis and grading. If you miss the deadline for this
similarity report check, you have negated your chance to repair any inadvertent
plagiarism. All papers submitted to the graded genetic disease file at turnitin.com will be
the version that is graded, no exceptions. Any and all plagiarism (as evaluated by the
instructor) will be construed as intentional plagiarism, regardless of whether or not you
utilized the similarity report check upload or not. If you fail to upload your paper to the
graded genetic disease file at turnitin.com by the due date outlined in the attached
course schedule, you will receive a ZERO for the assignment, no exceptions. Make
sure you can submit properly by turning in a draft by April 12th. I will not be able to
assist you on last minute efforts!
Research Paper Sample Content Preview:
Parkinson`s Disease
Introduction
Parkinson`s disease is a degenerative disorder of the neurons. It is commonly seen in geriatrics aged 60 and above. More common forms of Parkinson`s disease are idiopathic, with only rare cases related to familial forms (Matsuda et al. 211). There is yet a known cause for Parkinson`s disease and researches are still ongoing to learn more about the disease. In fact, previous studies have found that formed aggregates of α-synuclein cause the loss of dopaminergic neurons in an area of the brain called the substantia nigra (Winner et al. 4194). The loss of such neurons was found to result to the familiar symptoms of Parkinson`s disease, which are bradykinesia, tremors and postural instability (Mizuno et al. 22215). However, recent studies have identified certain genes to be crucial factors in the pathogenesis of this neurodegenerative disorder (Matsuda et al. 211). These genes have been identified as PINK1 (PTEN-induced putative kinase 1) and Parkin(Matsuda et al. 211; Deng et al. 14503). This paper will discuss updates related to Parkinson`s disease as observed in the identification of the genesPINK1 and Parkin.
Parkin in Mitochondrial Autophagy
An experimental study performed by Narendra et al. (795) aimed to prove the relationship between the ligaseParkin and mitochondrial autophagy. Narendra et al. (795) stated that Parkinson`s disease is related to a mutation in Park2, which is a gene that codes for Parkin. This is also the gene that is responsible for the recessive inheritability of the disease. Parkin is believed to preserve the membrane and functions of mitochondria. Therefore, Parkin is responsible for removing dysfunctional mitochondria from cells. The study of Narendra et al. (795) held the purpose of demonstrating the relationship of Parkin to the functions of mitochondria since the buildup of degraded mitochondria was believed to lead to the loss of neurons, which is a characteristic of Parkinson`s disease (Narendra et al. 802). The researchers employed the use of HEK293 cells, which were treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP) (Narendra et al. 795). CCCP is a compound, which relatively produces damage to mitochondria. The researchers found that upon degradation of the mitochondria, certain amounts of Parkin were identified in the bulk of cells. The appearance of Parkin in cells wasfurther identified and quantified through Western Blot, and MitoTracker red among others (Narendra et al. 801). The researchers then concluded that a deficiency of Parkin leads to the loss of neurons seen in Parkinson`s disease. Moreover, the researchers concluded that Parkin is responsible for ensuring autophagy of dysfunctional organelles.
PINK1 in Mitophagy
In another experimental study (Matsuda et al. 211), the researchers reinforced Narendra et al.`s findings regarding the f...
Introduction
Parkinson`s disease is a degenerative disorder of the neurons. It is commonly seen in geriatrics aged 60 and above. More common forms of Parkinson`s disease are idiopathic, with only rare cases related to familial forms (Matsuda et al. 211). There is yet a known cause for Parkinson`s disease and researches are still ongoing to learn more about the disease. In fact, previous studies have found that formed aggregates of α-synuclein cause the loss of dopaminergic neurons in an area of the brain called the substantia nigra (Winner et al. 4194). The loss of such neurons was found to result to the familiar symptoms of Parkinson`s disease, which are bradykinesia, tremors and postural instability (Mizuno et al. 22215). However, recent studies have identified certain genes to be crucial factors in the pathogenesis of this neurodegenerative disorder (Matsuda et al. 211). These genes have been identified as PINK1 (PTEN-induced putative kinase 1) and Parkin(Matsuda et al. 211; Deng et al. 14503). This paper will discuss updates related to Parkinson`s disease as observed in the identification of the genesPINK1 and Parkin.
Parkin in Mitochondrial Autophagy
An experimental study performed by Narendra et al. (795) aimed to prove the relationship between the ligaseParkin and mitochondrial autophagy. Narendra et al. (795) stated that Parkinson`s disease is related to a mutation in Park2, which is a gene that codes for Parkin. This is also the gene that is responsible for the recessive inheritability of the disease. Parkin is believed to preserve the membrane and functions of mitochondria. Therefore, Parkin is responsible for removing dysfunctional mitochondria from cells. The study of Narendra et al. (795) held the purpose of demonstrating the relationship of Parkin to the functions of mitochondria since the buildup of degraded mitochondria was believed to lead to the loss of neurons, which is a characteristic of Parkinson`s disease (Narendra et al. 802). The researchers employed the use of HEK293 cells, which were treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP) (Narendra et al. 795). CCCP is a compound, which relatively produces damage to mitochondria. The researchers found that upon degradation of the mitochondria, certain amounts of Parkin were identified in the bulk of cells. The appearance of Parkin in cells wasfurther identified and quantified through Western Blot, and MitoTracker red among others (Narendra et al. 801). The researchers then concluded that a deficiency of Parkin leads to the loss of neurons seen in Parkinson`s disease. Moreover, the researchers concluded that Parkin is responsible for ensuring autophagy of dysfunctional organelles.
PINK1 in Mitophagy
In another experimental study (Matsuda et al. 211), the researchers reinforced Narendra et al.`s findings regarding the f...
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