Download Guidelines for the report

Guidelines for the report
1) It is assumed that in High School you learned how to write informal papers such as
essays about your personal experiences, and website or magazine-style articles. This
report is to learn how to write a literature review paper for publication in a scientific
journal. Therefore, do not write an informal report; make it professional. That means that
you should not use personal pronouns (I, me, you).
2) Topic: select a topic that has only 3-5 subheadings. That is all you will need for a small
paper like this. Email the title and subheadings, along with at least 3 of your references in
proper bibliography format by the due date listed on the syllabus. One of the three you
send me at this early due date should be a journal reference so I can make sure you are
citing your references properly.
3) Formatting
a. Use Times New Roman, 12 point font
b. The report should be 5-7 pages of text (not including any figures you wish to
insert). This does not include the title page (put your name on that and the title of
the paper) or the bibliography section.
c. The report should be double spaced. To do this, select all the text, go to the
paragraph tab, and select “double space” instead of using the enter key to make an
extra space. That way, I don’t have to fix all the lines again when I insert
comments.
d. Paragraphs should be indented 5 spaces. Do not leave a blank line between
paragraphs.
4) Do not use colloquial phrases (slang). That is not appropriate for formal writing.
Examples are:
“In other words….”
“On the other hand…”
“America’s love affair with drugs…”
“It has morphed into ….”
“…and the like”
“reckless abandon”
“probably around 4 times a day”
“Another preventative tip is…”
5) Don’t use the same unusual word twice in one sentence. Use a thesaurus to find another
word.
“Long-term use causes long-term alterations…”
6) Avoid using quotes. Rephrase the author’s words instead.
7) Within the body of the paper, many sentences will need citations. To do this, write the
author’s last name and year of publication (Smith 2010). If you want to use Smith’s 2010
article for a number of citations, break them up like this:
According to Smith (2010), such and such, blah blah blah. Smith also stated that
blah blah. Furthermore, Smith’s 2010 study indicated such and such.
You should then add a few sentences on the same issue from a different source.
Then you can go back to writing a few more sentences from Smith’s article if you
want.
If there are two authors, write (Smith and Jones 2010).
If there are three or more authors, write (Smith et. al 2010)
Notice that “et” has a period after it and “al” does not, and that both words are
italicized.
Do not use this phrase: “Research shows that….”
You should say “Smith (2010) states that….”
8) You must use at least 5 different sources for your citations. At least one must be a
published article in a scientific journal. GoogleScholar.com is one way to search for those
articles.
9) How to write a reference for your bibliography: Below are examples of how to cite a
book, journal, conference, and webpage.NOTE: Do not write the words "Journal" and
"Webpage" above each reference; just list them one after the other, with one space
between.
A good place to search for journal articles is here http://scholar.google.com/
BOOK
Abbott, I. A. and G. J. Hollenberg. 1976. Marine algae of California. Stanford University Press,
Stanford.
JOURNAL
Antoniou, M. G., A. A. Cruz, and D. D. Dionysiou. 2005. Cyanotoxins: New Generation of
Water Contaminants. J. Envir. Engrg 131:1239-1243.
NOTE: Eliminate this line if a journal lists the date of issue like this
doi:10.1111/j.1755-148X.2010.00791.x
CONFERENCE
Bennett, C. M. 1997. The role of ponds in biodiversity objectives: A case study on Merseyside,
Proceedings of the IK conference of the Pond Life Project. September 1997.
WEBPAGE
EPA.gov. 2010. Classification of lakes and ponds. Retrieved from
http://www.epa.gov/bioiweb1/aquatic/classify.html on January 17, 2011.
WEBPAGE WITH NO AUTHOR LISTED
Medical.net (2011). What are embryonic stem cells? Retrieved from http://www.newsmedical.net/health/What-are-Embryonic-Stem-Cells.aspx on March 17, 2012.
10) For those of you who submit reports by email, I will electronically edit the document.
You will see a tracking pane to the right with my comments, plus any changes I make in
the document are in color. There will also be little vertical black lines on the left side so
you can see where small edits were, such as commas and spaces added to omitted. To
remove these edit marks, open the document and click on the REVIEW tab at the top, and
in the "Changes" area click "Next", then "Accept". That will return your paper to looking
normal.
11) For your 15-minute report presentations, just read your report. If you want to bring a PPT
to go with it, that would be great. Everyone in the audience should either ask questions or
write down your comments about what you liked about the presentation or what the
person could have improved on. If you choose the written method, email them to me later
or give them to me on paper. These comments are worth 10 points for each of the two
days of presentation (20 points total).
Samples of two great papers are shown next:
Cutaneous Melanoma
John Doe
National University
Cutaneous melanoma develops in melanocyte cells, which are found in the epidermis
layer of skin. These cells produce a pigment called melanin and function as a protective layer
from the sun’s harmful UV rays. (Balch et al 2009). Throughout the world, it is estimated that
200,000 people were diagnosed with melanoma in 2008, with the majority of those diagnosed
being women (CRUK 2011a). Of the cancers seen in females between the ages of 20-40,
melanomas account for 12% (Coelho, S. G., & Hearing, V. J. 2010). However common amongst
women, it is found that more men die from melanoma, possibly due to an increased delay in
diagnosis and treatment (CRUK 2011a). Although melanoma is curable if diagnosed and treated
at an early stage, it is fatal in approximately 20% of patients diagnosed with the disease. (Balch
et al 2009). The prognosis is especially poor for metastatic melanoma, which is often seen in
younger patients, where treatment tends to be relatively ineffective (Mouawad et al 2010).
There are four main types of melanoma which present in patients, including Superficial
Spreading, Nodular, Lentigo Maligna and Acral Lentiginous. (Lens, M. 2008). The most
common type of cutaneous melanoma is Superficial Spreading melanoma. This type of
melanoma is responsible for nearly 70% of all melanomas found in Caucasians and is typically
found in populations in their late 40s and 50s, presenting in the lower extremities of females and
the trunk of males (Coelho, S. G., & Hearing, V. J. 2010). Superficial Spreading melanoma has
a tendency to originate in pre-existing naevus, moles, and is a slow growing cancer. People who
have a higher number of naevi are more likely to be at risk for this type of melanoma (Bataille et
al, 1996).
The second most common type of melanoma is Nodular Melanoma, which accounts for
10 to 15% of all melanomas found (Langley et al, 1998). Similar to Superficial Spreading
melanoma, Nodular melanoma typically found in middle aged people and is seen commonly on
the truck, as well as the neck and head. In contrast, Nodular melanoma is characterized by a
rapid growth and develops on normal skin, where there was no previous existence of a naevus
(Barnhill and Mihni, 1993). Lentigo Maligna melanoma represents for 5 to 10% of melanomas
and is found in older populations, most commonly those in their seventies. Unlike the previous
two type of melanoma, Lentigo Maligna is commonly found on the face, especially the cheeks
and nose, as well as the neck. These areas are indicative of long-term cumulative sun exposure,
which is the greatest risk factor for this type of melanoma (Cohen. 1995).
Acral Lentiginous melanoma assumes the remaining two to five percent of melanomas
and is found most commonly in Caucasians in their seventies. However, it is also present in dark
skinned populations as well. Of the melanomas that do occur in African-Americans, Asians and
Hispanics, Acral Lentiginous is present 30-70% of the time (Langley et al 1998). ALM is found
in areas of the epidermis where the stratum lucidum is present, such as on the palms of the hands
and soles of the feet. It is also found on under the nail plate, where it is referred to as subungual
melanoma (Barnhill and Mihm, 1993).
Though not a direct cause of melanoma, age and race typically are the strongest
indicators of one’s risk for developing melanoma, where risk increases with age and those with
red hair, blue eyes and fair skin, being at greatest risk (Diagnosis, 2011). Ultraviolet (UV)
exposure is considered the primary contributor of melanoma, especially in those exposed to high
levels as a child, those exposed to intermittent sun following a sunburn and foremost, those
exposed to UV-emitting tanning devices (Diagnosis, 2011).
Some theorize that UV exposure even in the earliest stages of life can have an impact on
ones likelihood for presenting with melanoma. The time of year, birth month specifically, may
even be a predictor of increased UV exposure at a vulnerable stage of life. Several studies
performed in the United States as well as in the United Kingdom indicate that exposure to UV
rays as early as in the first eight months of life, can indicate a greater risk of developing
melanoma later in life (Mack et al., 2010). Individuals born in March were found to have
statistically higher rates of melanoma, possibly due to an increased exposure to UV rays in the
seasons following their birth, as these months included warmer seasons with more sunshine
(Basta, 2011).
The American Joint Committee on Cancer Staging evaluates melanoma based on the
thickness of the tumor, which is considered the greatest indicator of survival, followed by the
presence of ulceration, infection of regional lymph nodes and distant metastases (Diagnosis,
2011). The importance of early detection of cutaneous melanoma is seen in the excellent
prognosis for early stage detection (Lens, 2008). Staging is based initially on tumor thickness,
where the tumor is measured from the granular cell layer to the deepest point of infection; this is
known as the Breslow thickness (Lens, M. 2008). Patients with non-ulcerated tumors that are
less than 2mm thick have Stage I melanoma and a five year survival rate of 90-95% (Diagnosis,
2011). Stage II involves ulcerated tumors or those with depths greater than 2mm, the five year
survival rate for patients in this group is 45 to 78%. Stage III melanomas involve node
metastases, survival rate for this group ranges between 30 and 70% based on the number of
positive lymph nodes (Diagnosis, 2011). The prognosis for Stage IV advanced melanoma is poor
and results in a median survival rate of 6 to 9 months (Lens, 2008). Stage IV melanoma is
diagnosed based on distant metastases, with the survival rate dependent on the location of these
metastases relative to vital organs (Diagnosis, 2011).
The critical time period from onset to diagnosis, lead Friedman et al (1985) to develop a
simple guide for individuals to follow distinguishing the early warning signs from normal
healthy skin. This mnemonic is commonly known as the ABCD’s, which refer to asymmetry,
border irregularity, color variation, diameter (Abbasi et al 2004). Later an “E” was added, which
represents an important “evolving” element to self-diagnosis, allowing one to identify the growth
as melanoma, rather than a benign naevus (Lens, M. (2008).
Once an initial diagnosis of melanoma has been made, for those patients with clinical
signs or symptoms of Stage III and IV metastatic disease, imaging studies such as chest X-rays,
ultrasonography, computed tomography, magnetic resonance imaging (MRI), positron emission
tomography (PET) and bone scintigraphy have proven useful in detecting metastasized
melanoma throughout the body (Choi and Gershenwald, 2007).
Surgical removal of the primary cutaneous melanomas is standard care, where a 1-2
centimeter of healthy skin surrounding the irregular skin is surgically removed (Lens, M. 2008).
Patients with clinical signs of regional nodal disease as a result of metastatic melanoma show
significant benefit from early surgical removal of the infected nodes (Lens, M. (2008). As a
postoperative follow up measure, laboratory evaluation of lactate dehydrogenase levels and liver
function are important indicators of recurrent disease (Lens, M. 2008). Carbon dioxide laser,
where a high-energy beam of light is administered to the tumor site for destruction of tumor
nodules, is the treatment of choice following a tumor recurrence after surgery has been
performed (Diagnosis, 2011). Another treatment, Sentinel Lymph node biopsy, is commonly
practiced in the United States in Stage III patients where tumor thickness is greater than 1 mm
(Lens, M. 2008).
Subsequent to surgical removal of tumor sites, alternative treatment for patients at high
risk of relapse, a high-dose of interferon-alpha (IFN- a) may be administered. This drug is
considered experimental in countries outside of the US, as the survival benefit is often
outweighed by the high toxicity levels and the cost of treatment (Lens 2008). However, isolated
limb infusion or perfusion of this high-dose chemotherapy drug may be carried out in specialist
centers when less invasive treatments are found to be ineffective (Diagnosis, 2011).
As melanoma is resistant to chemotherapy, experimental vaccine treatments are being tested and
combination therapy, although experimental, is considered the most optimistic form of treatment
for advanced stage patients (Lens, 2008). A combination chemotherapy drug for patients with
metastatic melanoma that is often used is Dacarbazine (Diagnosis, 2011). Adoptive cell therapy
is another experimental treatment and includes use of Ipilimumab, a monoclonal antibody that
augments T cell activation, and Vemurafenib, an inhibitor of mutated BRAF gene found in
melanoma cells (Diagnosis, 2011).
Once the disease has developed beyond Stage II and is no longer surgically salvageable,
survival rates significantly decline with care becoming simply palliative at Stage IV (Diagnosis,
2011). The greatest preventative measures that can be taken include avoiding direct UV
exposure, either from the sun or from tanning devices, and when exposure is unavoidable,
limiting exposure and protecting skin (Diagnosis, 2011). Studies in England have indicated a 5%
annual growth rate in the incidence of melanomas among young females (Basta, 2011).
Worldwide, the annual death toll for melanoma is 40,000, with the medial survival time at just
6.2 months (Natarajan, 2011). Education of the risks related to UV rays and prolonged sun
exposure, especially during peak sunshine hours and for fair skinned individuals. Prevention
may be one of the greatest differences that can be made in the spread of this disease. Early
detection of melanoma, once preventative measures have failed, give the patient the best chance
at survival.
References
Abbasi NR, Shaw HM, Rigel DS et al (2004) Early diagnosis of cutaneous melanoma: revisiting
the ABCD criteria. JAMA 292(22): 2771-6
Balch C, Gershenwald J, Soong SJ et al (2009) Final version of 2009 AJCC melanoma staging
and classification. Journal of Clinical Oncology. 27, 36, 6199-6206.
Basta, N. O., James, P. W., Craft, A. W., & McNally, R. Q. (2011). Seasonal variation in the
month of birth in teenagers and young adults with melanoma suggests the involvement of
early-life UV exposure. Pigment Cell & Melanoma Research, 24(1), 250-253.
doi:10.1111/j.1755-148X.2010.00791.x
Bataille V, Bishop JA, Sasieni P et a! (1996) Risks of cutaneous melanoma in relation to the
numbers, types, and sites of naevi: a case-control study. Br J Cancer 73(12): 1605-1l
Barnhill RL, Mihm MC Jr (1993) The histopathology of cutaneous malignant melanoma. Semin
Diagn Pathol 10(1): 47-75
Cancer Research UK (2011a) Skin Cancer – UK Incidence Statistics. http://info.
cancerresearchuk.org/cancerstats/types/skin/incidence/uk-skin-cancer-incidence-statistics
Coelho, S. G., & Hearing, V. J. (2010). UVA tanning is involved in the increased incidence of
skin cancers in fair-skinned young women. Pigment Cell & Melanoma Research, 23(1),
57-63. doi:10.1111/j.1755-148X.2009.00656.x
Choi EA. Gershenwald JE (2007) Imaging studies in patients with melanoma. Surg Oncol Clin N
Am 16(2): 403-3O
Diagnosis and management of malignant melanoma. (2011). Cancer Nursing Practice, 10(7), 3037.
Friedman RJ, Rigel DS, Kopf AW (1985) Early detection of malignant melanoma: the role of
physician examination and self-examination of the skin. CA Cancer J Clin 35(3): 130-51
Langley RG, Fitzpatrick TB, Sober AJ (1998) Clinical characteristics. In: Balch CM, Houghton
AN, Sober AJ, Soong S, eds. Cutaneous Melanoma. 3rd edn. Quality Medical Publishing,
St Louis: 82-101
Lens, M. (2008). Current clinical overview of cutaneous melanoma. British Journal Of Nursing
(BJN), 17(5), 300-305.
Lens MB, Nathan P, Bataille V (2007) Excision margins for primary cutaneous melanoma:
updated pooled analysis of randomized controlled trials. Arch Surg 142(9): 885-91
Mack, M.C., Tierney, N.K., Ruvolo, E., Stamatas, G.N., Martin, K.M., and Kollias, N. (2010).
Development of solar UVR-related pigmentation begins as early as the first summer of
life. J. Invest. Dermatol. 130, 2335–2338.
Natarajan, N., Telang, S., Miller, D., & Chesney, J. (2011). Novel Immunotherapeutic Agents
and Small Molecule Antagonists of Signalling Kinases for the Treatment of Metastatic
Melanoma. Drugs, 71(10), 1233-1250.
Purdue, M., Freeman, L., Anderson, W., & Tucker, M. (2008). Recent Trends in Incidence of
Cutaneous Melanoma among US Caucasian Young Adults. Journal Of Investigative
Dermatology, 128(12), 2905-2908.
Pulmonary Valve Stenosis
John Doe
National University
Pulmonary Valve Stenosis
Pulmonary valve stenosis is a condition in which there is an obstruction on or near the
pulmonary valve, hindering the flow of blood to the lungs. The pulmonary valve, located
between the right ventricle and pulmonary artery, consists of three leaflets of tissue arranged
in a circular formation. In a healthy adult, these leaflets are usually only a few millimeters thick.
With pulmonic stenosis, however, the leaflets have become abnormally thick or, in some cases,
fused together obstructing blood flow (Zipes, Libby et al 2007). This obstruction causes the
right ventricle to compensate by pumping harder usually resulting in right ventricular
hypertrophy and contributes to the poor perfusion of the rest of the body.
There are few identified causes for pulmonic stenosis but it is most commonly
considered a congenital disorder with some suspected genetic component. In some studies it
has been observed affecting different individuals from the same family between generations
(Campbell 1962). Pulmonic stenosis can result from two other conditions, however, namely,
carcinoid syndrome or rheumatic fever (Pellikka, Tajik et al). Carcinoid syndrome is a series of
symptoms resulting from the formation of carcinoid tumors. The tumors, normally found in the
digestive tract, produce an excess of the hormone serotonin. The excess serotonin promotes a
buildup of fibrous connective tissue in the cardiac valves, particularly on the right side of the
heart. This buildup obstructs the normal passage of blood through the pulmonary valve
resulting in its stenosis. The stenosis caused by rheumatic fever is a result from the
inflammation of the cardiac muscle and its valves as caused by streptococcus pyogenes or strep
throat. Aside from the previously mentioned factors, however, pulmonic stenosis does not
favor a particular demographic and is found across all socioeconomic boundaries (Campbell
1962).
Regardless of the cause, pulmonic stenosis normally presents in adults as chest pain,
fatigue, with poor weight gain, shortness of breath or edema of the lower extremities (Zipes,
Libby, et al 2007). Infants usually present with cyanosis and in older children with no visible
symptoms, it can be heard as a heart murmur (Campbell 1962). An electrocardiogram or
echocardiogram can both be helpful in identifying pulmonic stenosis but the definitive
identification of the stenosis is primarily determined through the use of an intravenous catheter
that measures the pressure of the right ventricle and the pressure of the pulmonary artery,
noting any significant difference between the two (Herrmann 1997).
Prior to the 1980’s the only way to treat pulmonic stenosis was with open heart surgery.
In the majority of cases, the surgery was reserved only for adult patients, and only under a very
specific set of circumstances. Generally, one or more of the leaflets in the valve was removed
to allow easier passage of blood or either the entire valve was removed and replaced with a
prosthetic (Kan, White et al 1982). However, with the introduction of balloon valvuloplasty in
1982, the medical community saw a tremendous opportunity to address cardiac disorders less
invasively. Since its advent, physicians have documented an overwhelming amount of cases in
which the procedure has been performed on both adults and adolescents with positive long
term outcomes (Rao, Patnana et al 1998).
Balloon valvuloplasty is performed by inserting a long sterile tube into the femoral
artery and channeling it to the heart. A series of catheters are then placed in the tube and fed
through it to the right ventricle. One catheter is used to obtain fluoroscopic images of the area
in order to assist physicians in visualizing the procedure but it is also used to determine the
diameter of the circular ring of tissue to which the leaflets are attached. The next is used to
measure the pressures in the right ventricle and pulmonary artery. The difference in pressures
is referred to as the valve gradient. The gradient of a healthy heart is normally below 50
mmHg. Moderate pulmonic stenosis is considered to have a valve gradient of 50-80 mmHg,
and severe pulmonic stenosis has a valve gradient of greater than 80 mmHg (Nugent, Freedom
et al 1977).
Once these measurements are taken, another series of catheters are inserted into the
tube and funneled to the pulmonary valve. These are the guide wires used to insert and
accurately place the balloon used to dilate the obstructed area. Once in place, the balloon is
inflated to the diameter of the valve. This may occur 2 or 3 times in order to ensure proper
dilation, possibly changing the size of the balloon to allow for a better fit (Kan, White et al
1982). After the balloon is deflated and removed from the tube, the original catheters are
reinserted to measure the new pressures of the right ventricle and pulmonary artery. If they
are acceptable, all the catheters, including the sterile tube is removed from the femoral artery
and the patient is monitored for the next 24 hours to ensure no complications arise from the
procedure (Rao, Patnana et al 1998).
Though the outcomes for balloon valvuloplasty are generally very positive, there are a
number of complications that may occur as a result of the procedure. The first and most
common complication relates to the pulmonary valve’s primary function. When the ventricles
contract, blood is pushed through the valve and into the pulmonary artery. In a healthy heart,
when the ventricles cease contracting, the leaflets of the valve immediately snap shut
preventing the backflow, or “regurgitation” of blood back into the ventricle. However, with
balloon valvuloplasty, because the balloon forcefully presses the leaflets against the wall of the
valve, the leaflets may not fit back together perfectly. This oftentimes results in some degree
of leakage where a small amount of blood is allowed regurgitate (Kan, White et al 1982).
However, many physicians consider this complication as more tolerable for the body long term
than an obstructed valve (Rao, Patnana et al 1998).
Two other risks associated with balloon valvuloplasty can be resolved fairly easily and
oftentimes resolves on its own. The first risk is the formation of blood clots during the
procedure. However, this risk is largely mitigated as a result of the use of blood thinners prior
to beginning the treatment. The second risk occurs as a result of the heart being irritated with
the introduction of the catheters. This may cause the heart rate to either slow down or speed
up. However, this problem does not last long and normally resolves itself (Kan, White et al
1982). Overall, the chance of any serious negative event, including death, related to the
procedure is estimated to occur in about one in every 50,000 procedures (Kuntz, Tosteson et al
1991).
If the pulmonic stenosis is not relieved by the valvuloplasty or if the degeneration of the
pulmonary valve is too great, a complete valve replacement may be necessary. Because heart
valve prosthetics have historically been in use long before the introduction of balloon
valvuloplasty, there tends to be a wide range of prosthetics on the market. The two main types
of prosthetics available are either mechanical or biological heart valves. The mechanical variety
has gone through a number of developments since their introduction in the 1950s. They began
as caged ball valves in the 50s and 60s, followed by the tilting disc valves in the late 60s and
early 70s, and finally the bileaflet valves that are still in use today (Zilla 2008). Similar to the
developments of the mechanical heart valves, biologic heart valves have gone through their
own evolution since their introduction in 1965. These valves can be fashioned from porcine
heart valves, which is most common, bovine heart valves, or, the still relatively rare, preserved
human heart valves (Pibarot, Dumesnil 2009). The foreign valves undergo a series of
decontamination processes which results in the elimination of all chemicals that the host body
may recognize as foreign (Chaikof 2007). This allows the host to be more receptive to the
prosthetic and in most cases is more readily accepted than their mechanical counterparts.
Both mechanical and biological prosthetic heart valves have benefits and drawbacks to
their use. The largest concern with mechanical heart valves is the formation of blood clots.
Though the mechanical valves are constructed with materials that are intended to minimize this
response, there is still a 1-2% risk of clot formation per year. In order to limit the risk even
further, the patient is required to be on anticoagulants for the duration of his or her life
(Pibarot, Dumesnil 2009). This risk, however, is often considered an acceptable one when
weighed against the benefit of durability. The functional duration of the mechanical valve as
compared to the duration of the biological prosthetic is a drastic one. Though the human body
may respond better to a biological prosthetic, the functional duration of it tends to cease
around the 10 year mark (Cohn, Collins et al 1981). Mechanical prosthetics tend to last
upwards of 20 years (Pibarot, Dumesnil 2009). This factor makes mechanical prosthetics ideal
for younger adults with a potentially longer need for valve function but less ideal for the elderly
or pregnant women. This demographic tends to be unable to be on a regimen of blood thinners
for an extended period of time and coupled with the diminished need for a prosthetic to
function longer than 10 years. The use of biological prosthetics is more prevalent in these
instances.
With the great success of balloon valvuloplasty, the need for surgical intervention has
largely declined. Following either balloon valvuloplasty or valve replacement, patients will need
to continue to see a cardiologist for annual check-ups. But with the high rate of success and
minimal residual regurgitation, a far majority of patients have been documented to go on and
lead normal lives.
Bibliography
Campbell, M. 1962. Factors in the aetiology of pulmonary stenosis. Br Heart J 24:625.
Chaikof, Elliot L. 2007. The Development of Prosthetic Heart Valves – Lessons in Form and Function. N
Engl J Med 2007; 357:1368-1371.
Cohn, Lawrence H., Collins, John J., Gilbert, H. Mudge, and Pratter, Frederick. 1981. Five to Eight – Year
Follow –up of Patients Undergoing Porcine Heart – Valve Replacement. N Engl J Med 304:258-262
Herrmann, HC. 1997. Mitral, pulmonic, tricuspid, and prosthetic disease. In: Cardiac catheterization:
Concepts, Techniques, and Applications, Uretsky, BF (Ed), Blackwell Science, Boston
Johnson, LW, Grossman, W, Dalen, JE, et al. 1972. Pulmonic stenosis in the adult: Long-term follow-up
results. N Engl J Med 287:1159.
Kan, JW, White, RI Jr, Mitchell, SE, et al. 1982. Percutaneous balloon valvuloplasty: A new method for
treating congenital pulmonary-valve stenosis. N Engl J Med 307:540.
Karbhase J.N., Rachmale G.G., Panday S.R. 1980. Use of indigenous pig pericardial valves for mitral valve
replacement. J Postgrad Med 26:178-180A
Kuntz RE, Tosteson AN, Berman AD, Goldman L, et al. 1991. Predictors of event-free survival after
balloon aortic valvuloplasty. N Engl J Med 325: 17-23.
Nugent, EW, Freedom, RM, Nora, JJ, et al. 1977. Clinical course in pulmonic stenosis. Circulation 56:I.
Pediatric Cardiology, 2007. Pulmonary Stenosis. Retrieved from
http://pediatriccardiology.uchicago.edu/mp/chd/ps/ps.html on March 20, 2012.
Pellikka, PA, Tajik, AJ, Khandheria, BK, et al. 1993. Carcinoid heart disease: Clinical and
echocardiographic spectrum in 74 patients. 87:1188.
Pibarot P, Dumesnil JG. 2009. Prosthetic heart valves: selection of the optimal prosthesis and long-term
management. Circulation. 119(7):1034-48
Rao, PS, Patnana, M, Buck, SH, et al. 1998. Results of three to 10 year follow up of balloon dilatation of
the pulmonic valve. Heart 80:591.
Vongpatanasin W, Hillis LD, Lange RA. 1996. Prosthetic heart valves. N Engl J Med. 335(6):407-16.
Zipes DP, Libby P, Bonow RO, Braunwald E, eds. 2007 Braunwald's Heart Disease: A Textbook of
Cardiovascular Medicine. 8th ed.
Zilla. 2004. "Bioprosthetic Heart Valve." Encyclopedia of Biomaterials and Biomedical Engineering 1:
722-736