What book, movie or song can I compare with "Zenas Witt" by Edgar Lee Masters?

One must first consider what Zenas's problem is:

I was sixteen, and I had the most terrible dreams,

And specks before my eyes, and nervous weakness.

And I couldn't remember the books I read...

And my back was weak, and I worried and worried...

Zenas sees eye floaters ("specks before the eyes"), has a poor memory, and worries obsessively. In my reading of the poem, I associate his symptoms with the onset of madness, particularly schizophrenia. It's important, too, that he is sixteen, as signs of schizophrenia usually arise when someone is in their late-teens or early-twenties. 

He "worried" more after reading "Dr. Weese's advertisement," which outlined all that was wrong with him and predicted "an early grave." Perhaps Zenas read that he was likely to commit suicide. 

In the end, he does not die of this, but of "a cough," probably tuberculosis. In death, he is relieved of the "terrible dreams."

If you choose to use this reading of the poem in your paper, there are a myriad of comparisons you can make. I will list a few in each form of media that you have mentioned.

Books: Girl, Interrupted; One Flew Over the Cuckoo's Nest

Movies: If you do not care to read the aforementioned books, both were turned into films. If you like classic films, check out The Snake Pit starring Olivia de Havilland, one of the first Hollywood films to deal with the subjects of mental illness and treatment. 

Song: "Christine" by Siouxsie and the Banshees. Pay particular attention to the following lyrics: "She tries not to shatter / Kaleidoscope style...This big-eyed girl sees her faces unfurl / Now she's in purple, now she's the turtle / Disintegrating..."

I hope this helps. 

Does the perilymph help with balance, hearing, or both?

The inner ear has two functional parts: the vestibular complex which is responsible for the sense of balance and the cochlea which is responsible for hearing.

It is made up of a series of tubes in the temporal bone of the skull. The inner surface of this bony tube is called the bony labyrinth. The bony labyrinth encloses a membranous structure which is called the membranous labyrinth.

Between the inner surface of the bony labyrinth and the outer surface of the membranous labyrinth is a space, the perilymphatic space, which is occupied by a fluid called the perilymph. The inner part of the membranous labyrinth contains a different type of fluid called the endolymph.

Anatomically, the bony labyrinth can be segmented into three areas, the vestibule and the semi-circular canals, both of which make up the vestibular complex and a third segment which is a spiral-shaped chamber which houses the cochlear duct. Receptors within the cochlear duct provide the sense of hearing.

On each side of the cochlear duct is a perilymph filled canal, the tympanic and the vestibular canals through which pressure changes caused by sounds entering the ear travel down to the cochlear. These pressure changes stimulate receptor cells in the cochlear to produce electrical impulses through a process called transduction. These signals travel to the brain via the auditory nerve to be interpreted as sound.

The perilymph surrounds and cushions the membranous labyrinth in the vestibular system but it does not participate directly in the sense of balance.

What is Zellweger syndrome?

Risk Factors

The ZSS disorders are inherited in an autosomal recessive manner. Individuals
with mutations in both copies of any one of the twelve different
PEX genes known to be associated with ZSS disorders are
affected. Full siblings of these individuals have a 25 percent risk of being
affected, a 50 percent risk of being an asymptomatic carrier, and a 25 percent
chance of being unaffected and not a carrier. Male and female infants are affected
with equal frequency. Cases of ZSS disorders have been observed worldwide; no
particular ethnic preponderance has been noted.

Etiology and Genetics

Peroxisomes are small, membrane-bound organelles found in
cells throughout the body. They are involved in a variety of metabolic processes,
including the breakdown of toxic substances, such as hydrogen peroxide, and the
production of bile acids, necessary for digestion of dietary fats. Peroxisomes are
also involved in degradation of very long chain fatty acids (VLCFAs) in a process
known as beta-oxidation, essential for energy production. Peroxisomes play a role
in the synthesis of certain types of lipids, such as plasmalogens, which are
important components of cell membranes in certain tissues (such as the brain).

Proteins necessary for peroxisome function and membrane formation are made within the cell, then transported into existing peroxisomes. Importing these essential proteins prompts growth and division, resulting in the formation of new peroxisomes. In the ZSS disorders, these proteins are unable to be transported into peroxisomes, resulting in decreased biogenesis and function.

ZSS disorders are caused by mutations in the PEX genes, which
encode these essential proteins, known as peroxins. Though approximately
twenty-nine PEX genes have been identified, ZSS disorders have
been associated with mutations in only twelve (located at the following
chromosomal positions): PEX1 (7q21q22) PEX2 or
PXMP3 (8q21.1), PEX3(6q23q24),
PEX5(12p13.3), PEX6 (6p21.1),
PEX10(1p36.32), PEX12 (17q12),
PEX13(2p15), PEX14(1p36.2), PEX16
(11p12p11.2), PEX19 (1q22), and PEX26
(22q11.2). In some cases, the particular gene involved and the type of mutations
present are predictive of the ultimate effect on biogenesis and can be associated
with clinical severity. Mutations in PEX1 is the most common
cause of ZSS, affecting nearly 70 percent of individuals with the disease.

Symptoms

Though once considered separate entities, it is now known that Zellweger
syndrome (ZS), neonatal adrenoleukodystrophy (NALD), and infantile
Refsum
disease (IRD) share a common etiology and represent differing
degrees of severity along the Zellweger syndrome spectrum. There is little
distinction between these conditions, although historically, severely affected
infants were characterized as having ZS and those surviving more than one year and
making some type of developmental progress were thought to have NALD or IRD.

The ZSS disorder typically appears during childhood; though extremely rare,
presentation in adulthood has been reported. Affected neonates often present with
severe hypotonia, failure to thrive, seizures, and liver dysfunction. Some
are noted to have distinctive facial features and neuronal migration defects. Bony
stippling may also be seen on radiographs. Older children may have additional
issues such as hearing loss and/or retinal dystrophy. Affected individuals are
noted to have decreased levels of docosahexaenoic acid (DHA), thought to be
important in brain development, as well as decreased bile acids, important in
normal digestion. Liver dysfunction can result in coagulation
problems, and renal failure, thought to be due to renal cysts,
can also occur. Severely affected individuals usually make no developmental
progress; individuals with milder disease have a wide range of intellectual
abilities, with most exhibiting developmental delays. Loss of previously acquired
skills occurs in some due to progressive leukodystrophy.

Screening and Diagnosis

Analysis of levels of VLCFAs in the plasma is a useful initial screening test. Affected individuals typically have elevated concentrations of C26:0 and C26:1 and elevated C24/C22 and C26/C22 ratios. Measurements of plasmalogens, phytanic and pristanic acids, pipecolic acid, and plasma bile acids are also helpful in diagnosing ZSS and distinguishing this from other peroxisomal disorders. Confirmation of abnormalities noted on blood samples should be performed on cultured fibroblasts. Documentation of causative mutations in one of the PEX genes associated with ZSS can also further confirm the diagnosis.

Treatment and Therapy

Treatment for ZSS disorders remains largely symptomatic. Supplying an adequate
caloric intake may require the placement of a gastrostomy tube. Supplementation of
vitamin
K and other fat-soluble vitamins is recommended. Hearing aids
are used to address hearing loss. Antiepileptic drugs may be used to control
seizures. Supplementation with bile acids, deficient in ZSS, is currently under
investigation. Supplemental DHA has been proposed as a treatment for ZSS, but its
clinical effects have not been proven. Liver transplantation has been attempted in
few cases, though long-term clinical outcomes are currently unavailable.

Prevention and Outcomes

Most severely affected individuals die before one year of age. Evidence
suggests that of those who survive beyond this point with an apparently stable
course, most will survive through early childhood, and survival into young
adulthood has been documented. Death in older individuals is typically the result
of respiratory complications and/or renal failure.

There is no effective means of prevention for the ZSS disorders. Prenatal
testing is typically available for those in which the causative mutations in the
index case have been identified or the biochemical abnormalities have been
demonstrated on cultured fibroblasts. Individuals with a family history of these
disorders should be offered genetic counseling.

Bibliography

Poll-The, B., et
al. “Peroxisome Biogenesis Disorders with Prolonged Survival: Phenotypic
Expression in a Cohort of 31 Patients.” American Journal of Medical
Genetics 126A.4 (2004): 333–38. Print.

Rahim, R. S., A. C. B. Meedeniya, and D. I.
Crane. "Central Serotonergic Neuron Deficiency in a Mouse Model of Zellweger
Syndrome." Neuroscience 274 (2014): 229–41.
Print.

Steinberg, S., et
al. “Peroxisome Biogenesis Disorders.” Biochimica et Biophysica
Acta 1763 (2006): 1733–1748. Print.

Steinberg, Steven J., et al. "Peroxisome
Biogenesis Disorders, Zellweger Syndrome Spectrum."
GeneReviews. University of Washington, 10 May 2012. Web.
4 Aug. 2014.

Tran, Christel, et al. "Late-Onset Zellweger
Spectrum Disorder Caused by PEX6 Mutations Mimicking X-Linked
Adrenoleukodystrophy." Pediatric Neurology 51.2 (2014):
262–65. Print.

Wanders, R., et al.
“Peroxisomal Disorders I: Biochemistry and Genetics of Peroxisome Biogenesis
Disorders.” Clinical Genetics 67.2 (2005): 107–33.
Print.

What are bile and villi? What is their use in the digestive system?

Bile is a substance produced by the liver and stored in the gall bladder—a small organ attached to the liver.

The purpose of bile is to allow digestive enzymes called lipases to be able to hydrolyze or break down fats.  When a meal is eaten, bile stored in the gall bladder is released and enters the small intestine via the bile duct. In the presence of fat molecules, it acts to break up these large molecules into smaller droplets in a process called emulsification.  This allows more surface area for fat enzymes (lipases) to act on aiding in the process of digestion.

Villi are tiny finger-like projections found in the lining of the small intestine. Their purpose is to aid in the absorption of the end products of digestion. These tiny projections greatly increase the surface area for absorption of nutrients into the circulating blood and lymph systems. The villi are one-cell thick, which allows for diffusion to occur. Capillaries within the villi absorb amino acids and monosaccharides while the lacteals inside the villi absorb the end products of fat digestion. Capillaries are tiny blood vessels and lacteals are part of the lymph system. Eventually, all of the end products of digestion are circulated in the body and transported to the cells that need them.

I have included links showing the small intestinal lining and the anatomy of a villus.

What are squamous cell carcinomas?

Related condition:
Basal cell carcinomas

Definition:


Squamous cell carcinomas are malignant tumors that begin in the squamous cells that form the outer layer, or epidermis, of the skin.

Risk factors: Risk factors for squamous cell carcinomas include exposure to sunlight and ultraviolet radiation, age above fifty years, male gender, light-colored skin that burns easily, blue or green eyes, blond or red hair, residence in a geographical area that receives high sun exposure, repeated use of tanning beds, exposure to chemical carcinogens such as arsenic and tar, history of a large number of X rays, history of prior nonmelanoma skin cancer, and chronic immunosuppression.

Etiology and the disease process: Cumulative lifetime sun exposure is the main cause of squamous cell carcinoma. The shorter-wavelength portion of the ultraviolet spectrum (known as UVB) is believed to be about one thousandfold more active in inducing skin cancer than the longer-wavelength portion (known as UVA). Squamous cell carcinoma spreads faster than basal cell carcinoma (skin cancer that originates from basal keratinocytes in the epidermis) but still may be relatively slow growing. A subset of high-risk squamous cell carcinoma is capable of infiltrating the local area and metastasizing to regional lymph nodes as well as to distant locations and internal organs, most often to the lungs. This subset accounts for most of the morbidity and mortality associated with squamous cell carcinoma. The overall risk of metastasis for squamous cell carcinoma is about 5 percent, though factors such as tumor size, recurrence, and differentiation give some lesions higher risk.

Incidence: The annual incidence of squamous cell carcinoma in the United States is estimated to be over two million new cases per year. Because health registries often exclude squamous cell carcinoma from their databases and the rate of this cancer varies based on geographical location, this number is difficult to determine with accuracy.

Squamous cell carcinoma is the second most common form of skin cancer after basal cell carcinoma in whites. In people of African and Asian descent, squamous cell carcinoma, although relatively rare, is the most common form of skin cancer. Squamous cell carcinoma carries a higher mortality rate in blacks than in whites, probably because of delayed diagnosis, and occurs at a two to three times higher frequency in men than in women, presumably because of a higher cumulative exposure to sunlight.

There has been an apparent dramatic increase in the incidence of squamous cell carcinoma over the past several decades in the United States. This has been attributed to an increase in sun exposure in the general population, the advancing age of the population, and earlier diagnosis because of increased public awareness of skin cancer.

Symptoms: Squamous cell carcinoma may manifest as a variety of primary morphologies. The main symptom is a growing bump that may have a rough, scaly surface and flat, reddish patches. A sore that does not heal can be a sign of squamous cell carcinoma. Squamous cell carcinomas typically occur on portions of the skin that have been exposed to sunlight over a period of years; most lesions occur on the head and neck, especially the face, with the arms and hands the next most common locations. Histologically, a squamous cell carcinoma lesion involves the full thickness of the epidermis, but without involvement of the dermis, the deep vascular inner layer of the skin.

Screening and diagnosis: Screening for squamous cell carcinoma involves regular skin examinations for new lesions or changes in an existing lesion. Suspicious changes in an existing lesion include a change in appearance, color, size, or texture; pain; inflammation; bleeding; or itching. A lesion that is asymmetrical, has irregular or diffuse borders, has multiple colors, or is larger than six millimeters (mm) in diameter should be examined by a doctor.

The appearance of a skin lesion may indicate a squamous cell carcinoma, but a skin biopsy is required for a definitive diagnosis. The common types of biopsy are shave biopsy, punch biopsy, incisional biopsy (removes only a portion of the suspicious tissue), and excisional biopsy (removes the entire suspicious region). A biopsy for squamous cell carcinoma is normally done in the doctor’s office after the patient is given a local anesthetic. Biopsy samples must be deep enough to reach the mid-dermis to allow for determination of the presence or absence of invasive disease. For high-risk lesions, a larger tissue sample may be taken to assess the extent of invasion into nerves and to look for other features that would indicate a greater risk of metastasis.

Squamous cell carcinoma is staged according to the TNM staging (tumor/lymph node/metastasis) classification system. Because most squamous cell carcinomas are not metastatic at the time of diagnosis, the stage (T1-T4) is based on the size and characteristics of the lesion.

Treatment and therapy: Most squamous cell carcinomas are treated in the doctor’s office by cryotherapy (cryosurgery), electrodesiccation and curettage, excision with conventional margins, or Mohs micrographic surgery. It is important to remove the lesion completely in the first treatment because it can recur, metastasize, and cause death. More advanced or more invasive squamous cell carcinomas may require more aggressive treatment, including surgical management, radiation therapy, or both.

Cryotherapy with liquid nitrogen is a safe and low-cost procedure. Electrodesiccation and curettage, which may be used to treat squamous cell carcinoma on the trunk and extremities, is a simple procedure involving scraping and burning the tissue in the lesion. Its effectiveness is considered to be very dependent on technique; cure rates improve with a doctor’s experience. Excision with conventional margins (4 mm for lower-risk lesions is recommended) is highly effective for many squamous cell carcinomas. This technique commonly involves removal of a greater amount of normal tissue than is necessary for complete tumor removal. Mohs surgery, performed by dermatologic surgeons, allows for examination of the entire surgical margin during the procedure and the removal of the tumor in a step-wise procedure until clear margins are obtained. Mohs surgery is routinely performed as an outpatient procedure with the patient under local anesthesia and is widely available in the United States.

Nonsurgical treatment options for squamous cell carcinoma include topical chemotherapy and immune response modifiers (generally used for premalignant lesions), photodynamic therapy, radiation therapy (generally used in patients for whom surgery is not feasible and as an adjuvant therapy for patients with metastatic or high-risk squamous cell carcinoma), and systemic chemotherapy (for patients with metastatic disease).

Prognosis, prevention, and outcomes: Localized squamous cell carcinoma of the skin has a high cure rate if treated early. The overall five-year survival rate is estimated to be over 90 percent. For patients with no high-risk factors, this rate approaches 100 percent, and for patients with at least one high-risk factor, it decreases to around 70 percent. Risk factors associated with higher rates of recurrence and metastasis include tumors on the lips or ears; tumor size greater than two centimeters; an invasive, poorly differentiated, or recurrent tumor; nerve involvement; being an organ transplant recipient; having received chronic immunosuppressive therapy; and being infected with the human immunodeficiency virus (HIV) or having acquired immunodeficiency syndrome (AIDS).

Patients who develop one squamous cell carcinoma have a 40 percent risk of developing additional squamous cell carcinomas within the next two years and therefore should receive a complete skin examination every six to twelve months. Patients with high-risk tumors should receive complete skin and lymph node examinations every three to six months for at least two years.

The most important preventive measure is limiting exposure to sunlight. Skin should be protected by wearing protective clothing such as hats, long-sleeved shirts, long skirts, or pants. A high-quality broad-spectrum sunscreen that blocks UVA and UVB light should be applied at least thirty minutes before going outside and reapplied frequently. Exposure to the sunlight at midday when the sun is most intense should be limited.

Aboutalebi, S., and F. M. Strickland. “Immune Protection, Natural Products, and Skin Cancer: Is There Anything New Under the Sun?” Journal of Drugs in Dermatology 5.6 (2006): 512–17. Print.

Alam, M., and D. Ratner. “Cutaneous Squamous-Cell Carcinoma.” New England Journal of Medicine 344.13 (2001): 975–83. Print.

Clayman, G. L., et al. “Mortality Risk from Squamous Cell Skin Cancer.” Journal of Clinical Oncology 23.4 (2005): 759–65. Print.

Green, A., and R. Marks. “Squamous Cell Carcinoma of the Skin (Non-Metastatic).” Clinical Evidence 14 (2005): 2086–90. Print.

"Skin Cancer: Basal and Squamous Cell." Cancer.org. American Cancer Soc., 20 Feb. 2014. Web. 6 Jan. 2015.

"Squamous Cell Carcinoma of the Skin." Mayo Clinic. Mayo Foundation for Medical Education and Research, 27 Nov. 2014. Web. 6 Jan. 2015.

"Squamous Cell Carcinoma (SCC)." Skin Cancer Foundation. Skin Cancer Foundation, 2014. Web. 6 Jan. 2015.

Takata, M., and T. Saida. “Early Cancers of the Skin: Clinical, Histopathological, and Molecular Characteristics.” International Journal of Clinical Oncology 10.6 (2005): 391–7. Print.

What is the Human Genome Project?

Perspective

April 25, 1953, marked the publication of the double-helix model of DNA by James Watson and Francis Crick, based on the experimental data of Rosalind Franklin and others. It was fitting then, that fifty years later, in April of 2003, the complete sequence of the human genome was published, marking probably one of the greatest achievements in not only genetics but also all of science. In the years since then, thousands of scientists have been mining these data for information about the human body, how its genes shape development and behavior, and the role mutations play in diseases.

Origins of the Human Genome Project

The Human Genome Project (HGP) began as a result of the catastrophic events of World War II: the dropping of atomic bombs on the Japanese cities of Nagasaki and Hiroshima. There were many survivors who had been exposed to high levels of radiation, known to cause mutations. Such survivors were stigmatized by society and were considered poor marriage prospects, because of potential genetic damage. The US Atomic Energy Commission of the US Department of Energy (DOE) established the Atomic Bomb Casualty Commission in 1947 to assess mutations in such survivors. However, there were no suitable methods to measure these mutations, and it would be many years before suitable techniques would be developed. Knowing the sequence of the human genome would be the greatest tool for identifying human mutations.

Advances in Molecular Biology

As in all areas of science, progress in molecular biology was limited by available technology. Many advances in molecular biology made feasible the undertaking of the HGP. Starting in the 1970s, techniques were developed to isolate and clone individual genes. By 1977, Walter Gilbert and Frederick Sanger had independently developed methods for sequencing DNA, and in 1977, Sanger’s group published the sequence of the first genome, the small bacterial virus Phi X174. In 1985, Kary B. Mullis and colleagues developed the method of polymerase chain reaction (PCR), in which extremely small amounts of DNA could be amplified billions of times, providing significant amounts of specific DNA for analysis. Finally, in 1986, Leroy Hood and Applied Biosystems developed an automated DNA sequencer that could sequence DNA hundreds of times faster than was previously possible. Additional advances in computer technology made it possible to sequence the human genome.

The “Holy Grail” of Molecular Biology

In 1985 a conference of leading scientists was held at the University of California, Santa Cruz, to discuss the feasibility of sequencing the entire human genome. Biologists were looking for the equivalent of a Manhattan Project for biology. The Manhattan Project was the concerted effort of physicists to develop atomic weapons during World War II and resulted in huge increases of government funding for physics research. Walter Gilbert called the HGP the Holy Grail of molecular biology. With impetus from the DOE and the National Research Council, the Human Genome Project was launched in 1990 with James Watson as head. The goal of this project was to completely sequence the human genome of three billion base pairs by 2005 at a cost of $1.00 per base pair. In 1992, Watson resigned over a controversy surrounding the patenting of human sequences. Francis Collins
took over as head of the HGP at the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH). The sequencing of genetic model organisms, in addition to the human genome, was another of the goals of the NHGRI. This included genomes of the bacterium Escherichia coli, yeast, the fruit fly Drosophila melanogaster, the roundworm Caenorhabditis elegans, and other organisms. Moreover, 10 percent of the funding was to be directed toward studies of the social, ethical, and legal implications of learning the human genome.

Competition Between the Public and Private Sectors

J. Craig Venter, a former National Institutes of Health researcher, left the NIH and formed a private company, The Institute for Genomic Research (TIGR). TIGR, using a different approach (known as the shotgun method), was able to sequence the 1.8 million-base-pair genome of the first free-living organism, the bacteriumHaemophilus influenzae, in less than a year. In 1998, Venter along with Perkin-Elmer Corporation formed the biotech company Celera Genomics to sequence the human genome privately. Celera had more than three hundred of the world’s fastest automated sequencers and a supercomputer to analyze data. Meanwhile, public funds supported scientists in the United States, the United Kingdom, Japan, Canada, Sweden, and fourteen other countries working on HGP sequencing. The public sector was now in competition with Celera. To assure free access, each day new sequence data from the public projects were made available on the Internet.

The Human Genome Project Is Completed

In 2001, the first draft of the human genome sequence was published in the February 15 issue of Nature and the February 16 issue of Science. There are many short, repeated sequences of DNA in the genome, and certain regions that were difficult to sequence that needed to be sequenced again for accuracy, plus proofreading the sequence for errors in the process. Thus in April 2003, the final sequence of the human genome was achieved. It is remarkable that a government-funded project was completed two and a half years ahead of schedule and under budget, due to the ever increasing improvement of DNA technology and accuracy. April 25, 2003, was designated National DNA Day and has remained an annual day to educate the public, especially school-age children, about DNA and genetics in general.

Findings from the Human Genome Project

Perhaps the most surprising finding from the HGP is the relatively small number of human genes in the genome. Scientists had predicted the human genome would contain about one hundred thousand functional genes, yet the actual number of protein-coding sequences is approximately twenty-five thousand, representing only about 1 percent of the entire genome. In comparison, yeast has about six thousand genes, the fruit fly about thirteen thousand, and the Caenorhabditis about eighteen thousand. It was surprising that a complex human had less than twice the number of genes as the roundworm. The human genome also contains 740 genes that encode stable RNAs. The genome of the mouse, another model genetic organism, has providing interesting comparisons to the human genome.

Whose Genome Is It?

Although more than 99.99 percent of the DNA sequences of all humans are identical, 0.01 percent difference equals approximately 30 million base pair changes among individuals. One important question is, then, whose genome was sequenced? Venter has acknowledged that Celera has been sequencing mostly his DNA. However, the final sequence database is an “average” or “consensus” genome that is a conglomerate of many individuals contributing to the total sequence. Every human carries many and perhaps even hundreds of varying DNA changes. Even before the HGP was completed, databases listing single nucleotide polymorphisms were being established. These databases list the types of genetic variations that occur at individual nucleotides in the genome. For example, a cancer gene database lists the types of mutations that have been identified in specific cancer-causing genes and the frequency of such mutations. Mutations in genes such as BRCA1 and BRCA2
are responsible for breast and ovarian cancers, while mutations in the tumor-suppressor gene p53
have been found in the majority of human tumors.

The Future: Genomics and Proteomics

The Human Genome Project has given rise to two new fields of study. Genomics is the study of genomes. To do so requires databases and search engines to seek out information from these sequences. There are hundreds of such databases already established. Scientists can search for complete gene sequences if they know only a short segment of a gene. They can look for related sequences within the same genome or among different species. From such information one can study the evolution of particular genes.

The next step is to define the human proteome, giving rise to the field of proteomics. Proteomics seeks to determine the expression patterns of genes, the functions of the proteins produced, and the structure of specific proteins derived from their DNA sequence. If a particular protein is involved in a disease process, specific drugs to interfere with it may be designed.

Since 2003, many projects have developed to enhance our knowledge of the human genome. Two notable projects are the Cancer Genome Atlas and the Cancer Genome Anatomy Project . The goals of both projects are to determine the genes that underlie the cause of cancers, to find targeted gene therapy treatments, and to prevent those diseases. To date, several outcomes have become important to further progress in understanding the human genome, including the identification of 350 cancer-related genes and the establishment of publicly accessed databases of expressed sequence tags found throughout the genome.

With the success of the sequencing of the human genome has come the sequence completion of many more genomes of organisms, including the sequencing of the cow and dog genomes in 2004, five different domesticated pig breeds in 2005, and the domesticated cat in 2007, and the gorilla in 2012. The genomes of other strategically selected organisms have also been sequenced. The view of the National Human Genome Research Institute (NHGRI) is that to study essential functional and structural components of the human genome most effectively is to compare it with other organisms. Many of the selected organisms are in the mammalian order—for example, the giant panda, rabbit, and elephant. Also chosen, however, are nonmammalian organisms representing positions on the evolutionary time line that have been marked by important changes in anatomy, physiology development, or behavior. These organisms include slime mold, a ciliate, a choanoflagellate, a placozoan, a cnidarian (hydra), snails, roundworms, and lamprey eels.

Another great achievement of the HGP has been the acceleration of innovative technologies to use sequenced data. For example, copy number variants and single nucleotide polymorphisms (SNPs) are now being analyzed and used for the development of genetic tests that were unavailable before. Another technology, microarray analysis, utilizes the human genome to look at large numbers of small segments of DNA that, if mutated, may cause disease. Direct results of the Human Genome Project also include the International HapMap Project, the 1000 Genomes Project, and commercial "personal genotype sequencing." The study of the human genome has allowed scientists to make breakthroughs not only in the basic understanding of DNA and the genome but also in how the human genome changes with time and in individuals to cause disease and evolution. Humanity is just beginning to reap the benefits from the Human Genome Project.

Key terms



genome

:

the entire complement of genetic material (DNA) in a cell





genomics


:

the branch of genetics dealing with the study of genetic sequences





proteomics


:

the branch of genetics dealing with the expression, function, and structure of proteins




single nucleotide polymorphism (SNP)

:

differences at the individual nucleotide level among individuals





Bibliography

Choudhuri, Supratim. Bioinformatics for Beginners: Genes, Genomes, Molecular Evolution, Databases, and Analytical Tools. Burlington: Elsevier Science, 2014. Digital file.

Collins, Francis, and Karin G. Jegalian. “Deciphering the Code of Life.” Scientific American 281.6 (1999): 86–91. Print.

Dennis, Carina, and Richard Gallagher. The Human Genome. London: Palgrave, 2002. Print.

Hampton, Tracy. "Human Genome Initiatives Make Strides to Better Understand Health and Disease." JAMA: The Journal of the American Medical Association 309.14 (2013): 1449–51. MEDLINE with Full Text. Web. 25 July 2014.

Hyde, Michael J., and James A. Herrick. After the Genome: A Language for Our Biotechnological Future. Waco: Baylor UP, 2013. Print.

International Human Genome Sequencing Consortium. “Finishing the Eukaryotic Sequence of the Human Genome.” Nature 431 (2004): 931–45. Print.

International Human Genome Sequencing Consortium. “Initial Sequencing and Analysis of the Human Genome.” Nature 409 (2001): 860–921. Print.

Morris, Peter J. "From Mendel to the Human Genome Project." North Carolina Medical Journal 74.6 (2013): 477. MEDLINE Complete. Web. 25 July 2014.

Naidoo, Nasheen, et al. "Human Genetics and Genomics a Decade after the Release of the Draft Sequence of the Human Genome." Human Genomics 5.6 (2011): 577–622. MEDLINE Complete. Web. 25 July 2014.

Sulston, John, and Georgina Ferry. The Common Thread: A Story of Science, Politics, Ethics, and the Human Genome. Washington, DC: Joseph Henry, 2002. Print.

Wolfsberg, Tyra G., et al. “A User’s Guide to the Human Genome.” Nature Genetics Supplement 32 (2002): 1–79. Print.

What are some quotations from To Kill a Mockingbird?

It really depends on what theme or issue you are exploring, but there are some commonly quoted parts of the book.  Most of these relate to the theme of coming of age or injustice.  I have chosen some and explained them here.

The first significant quote is a conversation between Atticus and Scout.  Scout is upset by her teacher’s reaction to her at school.  She and Miss Caroline have many conflicts.  Atticus tries to teach Scout that sometimes the key to getting along with people is to try to see things from their perspective.

“First of all,” he said, “if you can learn a simple trick, Scout, you’ll get along a lot better with all kinds of folks. You never really understand a person until you consider things from his point of view-”

“Sir?”

“-until you climb into his skin and walk around in it.” (Ch. 3)

Empathy is an important lesson for any child to learn, and it is part of growing up.  It is especially important for Scout, because she will face some challenges soon.  Atticus knows this, and he tries to guide her in her interactions with others.

Another concept that is key to the novel is the concept of courage.  Scout and Jem will have to face injustice and come to an understanding of it as they get older and it gets closer to the trial of Tom Robinson.  Atticus tries to teach his children the importance of moral courage.  He explains to them that Mrs. Dubose was brave because she fought her illness and addiction.

I wanted you to see something about her—I wanted you to see what real courage is, instead of getting the idea that courage is a man with a gun in his hand. It’s when you know you’re licked before you begin but you begin anyway and you see it through no matter what. You rarely win, but sometimes you do. (Ch. 11) 

This is important because Scout and Jem will both have to understand that their father is brave for fighting for Tom Robinson against impossible odds. He wants them to understand why he is doing it, even though winning is unlikely.  He is setting an example for them that some things are worth doing even though they are hard.

When the children get guns for Christmas, Atticus explains to them that guns are not to be used to target the innocent.  Scout is surprised that her father says it is a sin to kill a mockingbird, because he never says anything is a sin.  She asks Miss Maudie, who explains what Atticus means. 

“Mockingbirds don’t do one thing but make music for us to enjoy. They don’t eat up people’s gardens, don’t nest in corncribs, they don’t do one thing but sing their hearts out for us. That’s why it’s a sin to kill a mockingbird.” (Ch. 10)

The mockingbirds are symbolic.  Scout realizes this later.  Mockingbirds do not harm anyone; their singing is only good for people.  They are easy targets.  Scout later realizes that people can be mockingbirds too, and society targeted Tom Robinson and Boo Radley for being different.