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THE SEARCHLIGHT MESSENGER
Student Post
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By: William Muncey; Edited By: Julienne Chase: Posted on Saturday, January 30, 2016 11:14 PM
 In the United States, The Affordable Care Act (ACA) is a
health care ordinance established by the federal government (it is commonly
referred to as Obamacare). The Act was adopted as a law by US President Barrack
Obama on March 23, 2010.
The goal of this law is to reform the United States
health systems by providing and improving access to quality and affordable
health care, health insurance, and providing American citizens with more rights
and protections by reducing health care expenditure for both individuals and
the government. The law also aims at expanding private and public insurance
coverage, as well as, regulating the insurance industry. It is a fantastic
thought, if it only worked as planned.
As we all know now, it is not completely as advertised. For
those of us in the middle class we have realized all too well that it crushes
us. It means more taxes. A staggering Five Hundred Billion Dollars in increased
taxes and fees. This is passed down to us through higher pricing on medical
expenses that we need.
You must purchase insurance, if you do not, your federal
income taxes will be penalized. You will no longer get the return that so many
count on every year. If you are covered with insurance through your employer,
you should tread lightly. Thirty-five million people could lose existing
coverage because the government has created incentives for employers to drop insurance
benefits.
There are higher premiums and costs associated with
the ACA. For a family of four earning ninety thousand dollars annually, take
home income would be about sixty-nine thousand dollars after local, state, and
federal taxes have been taken out. If these families lose their workplace
coverage and move into the exchanges, they could find themselves paying as much
as twenty-five percent of their take home pay on an average policy. That is a seventeen-thousand-dollar hit to their annual pay. That's the money they could have used to buy a car, save for college, or payoff their house.
Throughout my research I have interviewed
Doctor Kem Hor, Doctor Charles Counce, and have read many articles both for and
against ACA. I have also learned that the ACA really hurts Doctors. At the
beginning of 2014 it has dumped an additional twenty million Americans into
Medicaid. I personally had to start receiving Medicaid. What I have noticed, is
that it is very hard to find a Doctor who accepts new Medicaid patients, let alone see them at all. For
my family of five, that is very difficult. We have three younger
children who need medical attention from time to time, and it can be extremely
difficult to get them seen, sometimes taking up to a month to get an
appointment.
 Doctors feel overran by Medicaid patients. Some have stated
that they don’t have enough time with their patients any longer. It feels to some patients
that we are just a number. It shouldn’t be that way. Doctors are healers. Sometimes a little extra time with the patients can go a long way. Medicaid only
pays Doctors approximately fifty-six percent of what private insurance pays. [Understand that insurance systems are also a discount contracted with doctors to lower their fees to see a group of patients. This means that Doctors lose as much as eighty percent of their fee everytime they see a Medicaid patient. They can't even pay the overhead associated with the patient's visit.]
Doctors are put
in a tough spot, whether to accept Medicaid patients at a lesser rate or not
accepting Medicaid patients at all. America is projected to face a shortage of nearly ninety-two thousand doctors by the year 2020. Just here in the greater Colorado Springs area
there is a shortage of two hundred sixty doctors. Many surveys state that doctors have a
negative view on the ACA and its impact on the medical field. One survey found
that the ACA on top of all the other mandates like Tort Law costs, Skyrocketing Liability Insurance, this year's "ICD10", "CLIA", "OSHA", and "HIPAA" has become too much to bear, motivating forty-three percent of doctors to move up
their retirement within the next five years.
My overall thoughts on
this Affordable Care Act, is that it might be a good idea on paper, but after seeing it in action, it
has caused many more headaches than not. It has forced many doctors out of the
field to pursue other options. Doctors should not have to wait four to six months to
get paid by Medicaid or Medicare. I understand that doctors need to get paid for services
rendered in a timely fashion. They have bills as well as employees to pay, in addition to college and medical school tuition loan obligations and
bread for their table. It should not take patients a month to see a healthcare provider either.
 I have been waiting to see a specialist (a ninety minute drive north to Denver) for two and a half months now. The system is not working, and should never have been approved in its present form. Unfortunately, it is here to stay. So says the Supreme Court. We will all have to get used to it.
Obviously the Affordable Care Act does need a lot of improvements to actually do what it was meant to do, giving Americans better access to quality healthcare. [It has managed to do almost the opposite, by draining our pocketbooks, and scaring away the only people who can care for us.]
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Kayla Sa Pereira; Edited by Dr. C. M. Counce: Posted on Thursday, August 21, 2014 8:50 PM
 The
Milgram experiment is one of the most famous studies of obedience in psychology
to date. Begun in 1961, the experiment was done in order to better comprehend the acts of genocide committed by the Nazi’s in World War Two. Stanley Milgram, a psychologist at
Yale University, was the mastermind behind the study. The focus of the
experiment was “conflict between obedience to authority and personal
conscience”. Milgram wanted to explore the justifications of genocide based on
the testimonies given by the accused during the Nuremberg War Criminal Trials.
The accused claimed that they were just “following orders given by their
superiors”; this defense shaped the concept of the Milgram experiment.
Milgram began the experiment with a public announcement stating; “Persons needed
for a study of memory, we will pay you $4.00 for one hour of your time.” This
baited hook brought in over 600 people for Milgram to test and study. Once
people accepted the announcement they pulled straws to fill three roles; the
teacher, learner and the observer. Once the roles were distributed the
experiment could begin. Milgram started by having the teacher assist the
observer in connecting shock inducing electrodes to the learner. The teacher then
read off a list of words that the learner would have to memorize and repeat
back. If the learner gave any wrong answers, the teacher was instructed to
shock the learner. With every wrong answer given, the voltage of shock
increased; starting at 15 volts, and increasing by 15 volts until the voltage
reached 450. The shock machine in front of the teacher was set up like a switchboard.
The machine consisted of 30 switches with the voltage and description of shock placed
next to the switch. The 10 level or 150 volts was “strong shock”;
the 17 level or 255 volts was “intense shock”; the 25
level or 375 volts was “danger severe shock”; while the last two switches 435
volts and 450 volts were simply marked XXX standing for “ultimate pain”.
However,
while the teacher thought they were helping test the learner, the observer was
really testing the teacher. The learner and the observer were both part of Milgram’s
staff and were trained to act the part they played in order to get more
realistic results. The learner was not being shocked at all, but was cued to scream
in pain when the switches were flipped. If the teacher ever refused to flip the
switch, the observer was given four sayings to try and motivate the teacher to
continue. The first “motivator” was simple yet polite, “please continue”, after
that, they continued to get increasingly demanding; “the experiment requires
you to continue.”, “it is absolutely essential that you continue”, and lastly
“you have no other choice but to continue”. If the teacher refused to continue
after all four “motivators”, the experiment ended. If the teacher continued,
the experiment ended when 450 volts was reached. After the experiment concluded,
Milgram debriefed
the participants and scheduled a follow-up meeting with them. During the
debriefing the true nature of the experiment was revealed.
Milgram’s results
shocked him and the rest of the psychologists in his community. 65% of the
teachers completed the experiment by reaching 450 volts. All of the volunteers
continued the experiment to 300 volts. Milgram repeated the experiment 18 times
changing multiple variables in order to confirm the idea that it was human
nature to follow orders. With a change of location, obedience dropped to 47.5%. When
there was less personal responsibility, obedience increased to 92.5%. When the
teacher got physical with the learner, obedience dropped to 30%. When the
authority figure was giving orders from a distance, obedience fell to 20.5%.
 Milgram
was determined in researching how far people will go when listening and acting
upon instructions given to harm another human being in all different scenarios.
Milgram came to the conclusion that “Ordinary people are likely to follow
orders given by an authority figure, even to the extent of killing an innocent
human being. Obedience to authority is ingrained in
us all from the way we are brought up. People tend to obey orders from other
people if they recognize their authority as morally right and/ or legally right
based. This response to legitimate authority is learned in a variety of situations,
for example in family, school or work place.”
Milgram’s
experiment received, and continues to receive a great deal of criticism. In
1968, Orne and Holland made the statement that Milgram’s experiment lacked
“experimental realism”. Experimental realism is the
extent to which situations created in social psychology experiments are real
and impactful to participants. The concept of experimental realism was
developed in response to criticism; in that most social psychology experiments
take place in artificial laboratory settings, [and thus], are invalid for
examining how people truly think and act. Another complaint, was that Milgram’s
study was all Males, and the question still remains would the results stay the
same if females were tested. The final complaint was that Milgram’s experiment
cannot be seen as representative of the American population as his sample was
“self selected”. Meaning that the teachers of the experiment were all
responding to an advertisement found in the paper and are assumed to have a
volunteer personality which not everyone has.
Although the complaints about the experiment are valid, it
becomes very easy for others to point out the faults or mistakes in another’s
study. Experimental realism, although very useful, is hard to accomplish in any
study, in any field. The main problem comes down to weather the person being
studied is truly being honest during the study in which they are taking part.
This simply boils down to human error, because we can never truly know what
another person is feeling or thinking. While the second complaint seems
applicable, Milgram was doing the study based on the testimonies given by the
Nazi soldiers who were 90% Male. The new argument could be that Milgram should
have performed the study with 10% of the volunteers being women. However,
during World War II, it was said that Nazi women were not in the position to
harm, or given orders to harm anyone. If Milgram included women in the study,
the results would be worthless in inquiring whether the accused had a valid
defense. As for the volunteers, every experiment needs volunteers. No one can
make anyone do an experiment against their will. So, even with the volunteer
personality they will find the closest most realistic results that anyone would
be able to obtain in the given circumstance.
 While people will always have criticism, more people have
problems with the ethical issues behind Milgram’s study. Deception; the
teacher’s were unaware that they were not actually shocking the learner.
Protection of the participants; the teachers were exposed to tremendously
stressful scenarios that could have lead to psychological problems. The signs
of tension showed in the teachers; trembling, sweating, stuttering, laughing
nervously, and biting lips, while three teachers had uncontrollable seizures. Right
to Withdrawal; British Psychology Society states that, “the researchers should
make it plain to participants that they are free to withdraw from the experiment.”
With Milgram's four motivators, the psychology society feels that the teachers
were given no chance to withdraw from the experiment.
With every criticism that came Milgram's way, he had a retort.
As far as deception went, Milgram explained, “Illusion is used when necessary
in order to set the stage for the revelation of certain difficult-to-get-at-truths”.
When it came to the psychological well being of his volunteers, Milgram
debriefed them right after the experiment and set up an interview with them after
one year had past. After that year, over 80% of the volunteers had been “glad
to be a part of the experiment” while less than 2% wish they had never taken
part. The psychological well being of the volunteers is a big part of the
experiment. While no one wanted the volunteers to walk away with psychological
problems, it would have been a huge insight into the mind of a human who could
do harm to another human simply by “following orders”. After Milgram had debriefed
the participants at the end of the experiment, the stress levels and signs of
tension decreased dramatically. During the follow-up meeting a year later
Milgram noticed no long lasting psychological problems, so even with the risk
of psychological harm, it was necessary to the experiment.
The British Psychological Society says that everyone should have
the right to withdraw from an experiment. With the way Milgram's “motivators”
were phrased, the psychology community believes that they made it nearly
impossible for them to withdraw from the experiment. However, Milgram pointed
out that while the “motivators” might have made it difficult to withdraw from
the experiment, withdrawal was still possible, because 35% of the volunteers
withdrew from the study.
Ultimately, I find what Milgram did, to be very noble and risky;
he had conceived an idea for an experiment and executed it. For people, it is
easier to find flaws and mistakes in another’s work, instead of admiring the
process and guts it took to complete something new. I understand where the
psychological community is coming from and their concerns with all of the
ethical issues. In an ideal world the perfect execution of an experiment
wouldn’t have any ethical issues linked to it. However, we do not live in an
ideal world and sometimes to get to the dirty truth we have to play a little
bit dirty. I think for Milgram, this experiment was a huge success for
everything he believed in as a psychologist, and completely reflects his beliefs
in his career.
“Only in action can you fully realize the
forces operative in social behavior. That is why I am an experimentalist. For me
and my beliefs, I think that history repeats itself, and for us to be better
prepared for the future, we have to understand the past, making this study appropriate.
With technology and science where they are today, I see no better way to
execute this study. Maybe as imperfect beings we cannot create a perfect study,
but to stop trying because of obstacles makes us failures before we even have
the chance to succeed.” Milgram saw success through his obstacles and succeed
in accomplishing one of the most well-known social psychology studies of the twentieth
century.
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Tonya Meyerhoff: Posted on Saturday, May 19, 2012 4:04 PM
 From the first description of paralysis agitans in “An Essay on the Shaking Palsy” by James Parkinson in 1817 to the treatment of patients using levodopa developed by Arvid Carlsson, scientists and physicians have been working toward understanding and treating parkinsonian symptoms since the discovery of the disease. New research is furthering these goals by advancing the extent of knowledge needed to treat and eventually cure this disorder. Areas currently being studied include research into the development and progression of Parkinson’s disease (PD) with emphasis on the improvement of existing parkinsonian models and novel treatments including gene therapy and stem cells. Parkinson’s disease (PD) is a neurodegenerative disorder of the central nervous system with death of dopamineric cells in the substantia nigra creating common motor symptoms. One of the most difficult problems scientists have encountered with PD has been developing an animal model representative of the human disorder. Since PD is only known to occur in humans, researchers have been experimenting with recreating similar neurodegenerative damage in the rat brain with focus on the role of the protein α-synuclein. This protein is the primary structural component in Lewy bodies which are found inside nerve cells of a PD patient.
 Researchers Ulusoy, Decressac, Kirik, and Bjorklund (2010) have recently developed a more authentic model using adeno-associated virus (AAV) and lentivirus (LV) vectors to trigger overexpression of α-synuclein. These viruses have desirable characteristics for use as vectors in gene therapy as AAV infects humans but is not known to cause disease or integrate into the genetic material of the host and LV can transfer large amounts of genetic information into cells including non-dividing cells. By using these viral vectors to silence, express, or over express certain genes, scientists will be able to replicate PD models exhibiting damage and symptoms more analogous to the actual disease thereby creating a stronger correlation between successful research conducted on the animal model and the transference of this success to the actual patient.
 AAV has also been utilized in recreating dyskinesias, or involuntary movements, of PD patients. Cao, Yasuda, Uthayathas, Watts, Mouradian, Mochizuki, and Papa (2010) used AAV vectors to over express DeltaFosB. This transcription factor is found to be over expressed in the striatal neurons after chronic dopaminergic drug exposure and believed to be correlated with the PD patient’s diskinesias (Cao et al., 2012). Research supported their hypothesis leading to the speculation that, in future research, a decrease of the expression of this transcription factor could theoretically decrease certain PD patient symptoms.
Stem cell research, though controversial [in the recent past], is proving to be invaluable in the study of Parkinson’s disease. Mesenchymal stem cells from human umbilical cords can be easily obtained after birth while posing no risk to the infant. Recent discoveries involving mesenchymal stem cells comes from Xiong, Z. Zhang, Huang, Chen, Z. Zhang, Jia, Xiong, Liu, Cao, Liang, Sun, Lin, Wang (2011). These researchers transplanted modified stem cells into a hemiparkinsonian rat. The cells were modified with an AAV mediated delivery of human vascular endothelial growth factor (VEGF). VEGF is thought to be responsible for creating new blood vessels. The transplanted stem cells differentiated into dopaminergic neuron-like cells with the VEGF significantly enhancing this differentiation and reducing the loss of dopaminergic neurons in the substantia nigra (Xiong et al., 2011).
Other types of stem cell-based therapy involve human induced pluripotent stem cells (hiPCSs) which are similar to embryonic stem cells. HiPCSs, however, are derived from non-pluripotent cells, such as fibroblasts, by reactivation of pluripotent factors within the cell. Two common methods through which cells can be reprogrammed are viral or protein-based induced expression. Rhee, Ko, Chang, Yi, D. Kim, CH. Kim, Shim, Jo, BH. Kim, H. Lee, SH. Lee, Suh, Park, Koh, SH. Lee, Lanza, KS. Kim, and SH. Lee evaluated the safety of the different methods and found that virus-based hiPSCs exihibited early cell death and apoptosis during subculturing, a process in which cells are transferred to a fresh growth medium with the desire of prolonging life or increasing the number of cells in a culture (Rhee et al.’s, 2011). Protein-based hiPSCs, however, were expandable without senescence and were more similar to dopamine neurons. Furthermore, when transplanted these cells significantly reduced motor deficits in rats (Rhee et al., 2011).
As researchers begin to understand more about the development and progression of PD, attempts are being made to lessen or halt the pathogenesis of this disease. A particular area of study involves the tumor necrosis factor (TNF), a multifunctional, pro-inflammatory cytokine or signaling molecule. Researchers Harms, Barnum, Rhun, Varghese, Trevino, Blesch, and Tansey (2011) believe neuroinflammation from TNF may play a role in the pathogenesis of PD. Using lentivirus encoded to act in opposition to TNF, rats were injected in their lesioned substantia nigra to discover if TNF inhibition delayed neurodegeneration. Harms et al.’s (2011) were successful, leading to a discovery that might one day be used in a clinical setting to prevent dopaminergic neuron death and delay motor symptoms in the PD patient.
 Other methods of treating PD patients may eventually include axon regeneration. It has long been thought that the adult central nervous system is incapable of restoring axons. Kim, Chen, Oo, Kareva, Yarygina, Wang, During, Kholodilov, and Burke (2011) suggest that reactivating intrinsic cellular programs may allow for the regrowth of axons in the nigrostriatal projection. Using AAV transduction, activation of protein kinase AKT and Mtor resulted in regrowth of axons from dopaminergic neurons to the striatum. These results were confirmed by histological analysis and behavior recovery (Kim et al., 2011).
The treatment of PD may soon benefit from the innovative use of gene therapy. Neurologix Inc. is currently in an ongoing phase II clinical trial of NLX-P101 (Diaz-Nido, 2010). NLX-P101 is an AAV vector encoding for glutamic acid decarboxylase (GAD). As the PD patient suffers from dopamine depletion in the striatum, functional changes occur in the subthalamic nucleus (STN). This area becomes disinhibited and disrupts control of body movement. It is believed that GAD enhances inhibition of the neurotransmission from the STN thereby decreasing STN over activation. Neurologix Inc. conducted a previous phase I clinical trial demonstrating a reduction of motor deficits in animal models (Diaz-Nido, 2011). This treatment is being researched in the hopes of improving the functional ability of patients in the early stages of PD.
A similar trial involving AAV2-GAD to improve basal ganglia function in parkinsonian animal models was conducted by Lewitt, Rezai, Leehay, Ojemann, Flaherty, Eskandar, Kostyk, Thomas, Sarkar, Siddiqui, Tatter, Schwalb, Poston, Henderson, Kurlan, Richard, Van Meter, Sapan, During, Kaplitt, and Feigin (2011). These researchers conducted a double-blind, sham surgery, controlled randomized trial in which bilateral delivery of AAV2-GAD in the STN was compared with sham surgery patients. At the end of six months, the AAV2-GAD group showed significant improvement compared with the sham group (Lewitt et al., 2011). This study demonstrates the efficacy and safety of one method where gene therapy could be used for neurological disorders.
Late in the course of PD, patients become less responsive to dopaminergic therapy and experience an on-off phenomenon. An advanced PD patient will exhibit the on phase with excess abnormal movements and the off phase with prolonged immobility. Sustained levodopa treatment eventually increases a patient’s resistance to levodopa and the drug’s ability to control smooth muscle movement which results in this phenomenon. In an effort to help a patient with symptoms partially unresponsive to levodopa, researchers administered electroconvulsive therapy to patients in an effort to increase sensitivity of postsynaptic dopaminergic receptors (Perez, Valldeoriola, Fernandez-Egea, Sanchez, Rami, Tolossa, Muniz, Marti, & Bernardo, 2012). It was discovered that the treatment only showed significant differences in the number of freezing episodes if administered during the on phase of the phenomenon (Perez et al., 2012).
 Over the last two hundred years, researchers and physicians have been working diligently toward assisting those living with the cell death and motor symptoms of PD. The development of better animal models will help to devise treatment that is as applicable to a human as it is to the animal model from which it was researched. In addition, gene therapy and the use of stem cells can allow for future treatment of neurodegenerative cells with patient specific, engineered cells designed to restore areas of the brain damaged by dopaminergic neuron death. Therefore, despite its devastating effects, there is hope that with new advancements in the understanding and treatment of this disorder, patients in the future will have more options for living with or perhaps even curing Parkinson’s disease.
About the Author:
Tonya Meyerhoff, is an advanced Medical Laboratory Technology Student of Dr. Counce at the Intellitec Medical Institute. Tonya is admired by students and faculty alike. She is a true Lady and Scholar. The faculty of Intellitec Medical Institute expect great things from Ms. Meyerhoff, and would not be surprised to see her move toward a career in Medicine.
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Evamarie Hernandez, Medical Laboratory Technology Student: Posted on Monday, December 26, 2011 3:23 PM
Chronic Myelogenous Leukemia(CML) also referred to as Chronic Myeloid Leukemia, or Acute Granulocytic Leukemia, is a rare type of cancer involving the blood cells and bone marrow. It is found in white blood cells which contain the oncogene, Philadelphia Chromosome (Ph+). Unlike other Leukemias, this particular blood cancer tends to progress more slowly than acute forms of leukemia, is found more often in older adults, usually males 45 years of age and older, and rarely occurs in children. It should be made clear that the Leukemias are not inherited diseases, and as with all other Leukemias, in most cases of CML, a caus, cannot be identified, however, it is thought that CML may evolve from environmental risk factors such as ionizing radiation, certain viral attacks, and other environmental carcinogens. Chromosomes are the “set of instructions” for the body and control all the functions of cells. They are responsible for the production, division, and replication of daughter cells. These daughter cells should always have the correct replication of genetic programming (DNA), however, if there is something wrong with the chromosome then the “set of instructions” is also incorrect, and mutations can occur. Unique to CML is the Philadelphia Chromosome (Ph+). Discovered in 1960 in Philadelphia by Dr. Peter Nowell, this translocation defect was found as a consistent finding in CML. Due to the limited techniques available at the time, Dr. Nowell and his colleagues didn’t have the capability to find what happened to the genetic material in the translocation of the chromosomes. It was not until 1972 that Janet Rowley, MD, discovered the first known chromosomal translocation. It was then discovered that the Philadelphia chromosome (Ph+), forms when chromosomes 9 and 22 break and exchange portions as seen in the figure below.
What occurs then is a new set of abnormal instructions for the cells involved, in this case, the white blood cells, which no longer function properly. This results in the generation of an abnormal BCR-ABL gene which becomes oncogenetic (cancer-causing). This oncogenetic BCR-ABL gene causes a deregulation of the protein, tyrosine kinase. Tyrosine kinase functions as the “on/off” switch for cellular activity, and in this particular disease, the cell does not have a functional “on” switch for apoptosis (programmed cell death) which allows for the propagation of new and healthy generations of the white cell line. What this means is that these abnormal cells continue to replicate unchecked and proliferate in the bone marrow and body. These cells do not grow and die like normal cells and they overcrowd healthy cells and damage the bone marrow along with other organs. In addition to involving the bone marrow, CML can cause secondary problems, such as an enlarged spleen (splenomegaly) and liver (hepatomegaly).
CML does not always reveal itself with overt signs and symptoms during its early phases. A patient may have CML for some time before diagnosis. Some signs and symptoms of CML are: Easy bleeding Feeling fatigued Fever Frequent Infections Weight loss Loss of appetite Pain or fullness below the ribs on the left side Pale skin Night sweats CML can cause anemia and therefore fatigue because the unhealthy white blood cells are crowding out healthy red blood cells. At times, due to a shortage in healthy platelets (thrombocytopenia) which assist in controlling bleeding by helping to form clots, easy bleeding and bruising may occur. Conversely, an increased production of platelets (thrombocytosis) can cause excessive clot formation which may lead to cerebral vascular accidents (stroke) and myocardial infarction (heart attacks). Bone pain is not uncommon due to the neoplastic white blood cell build up in the bone marrow. The spleen becomes enlarged because the excess white blood cells are sequestered there. In some cases the spleen may become so enlarged it is at risk of rupturing. In addition, the white blood cells, although increased in number, and normally programmed to fight off infection, do not function properly, and the cells are unable to ward off infection. There are three phases of CML. They are: (1) The Chronic Phase, the initial early phase; (2) The Accelerated Phase, the transitional phase when the disease begins to become aggressive; and (3)The Blastic Phase, a severe malignancy which becomes life threatening. Each phase is measured proportionally by the amount of diseased cells versus healthy cells in the patient’s blood and bone marrow. With a higher proportion of diseased cells present, the more advanced the stage will be. Diagnostic work up for CML begins with a thorough history, and physical exam, checking for any lymphadenopathy (abnormalities in the lymph nodes), abdominal mass, or enlarged organs, evidence of ischemia, and of course, infection. Ancillary testing, including laboratory for a complete blood count, and blood chemistry are performed. Imaging, including chest x-ray and magnetic resonance imaging of suspicious sites are acquired. Finally, if CML is suspected, a bone marrow biopsy is performed. Confirmation ultimately utilizes laboratory testing for presence of oncogenetic markers including the Philadelphia chromosome and the BCR-ABL gene. Treatment for CML is targeted to eradicate as many blood cells that contain the abnormal BCR-ABL gene as possible. Treatment cannot rid the patient of all the abnormal cells but it can help achieve remission of the disease. There are specific drugs targeting the deregulated protein produced by the BCR-ABL gene, tyrosine kinase. Such medications are: Imatinib (Gleevec) Dasatinib (Sprycel) Nilotinib (Tasigna) Unfortunately, there is on occasion, no response to medication as the disease can become resistant to these interventions, in which case a blood stem cell transplant (bone marrow transplant) may offer a chance for patients. In bone marrow transplant therapies, high doses of chemotherapy are used to treat harvested blood forming cells in the bone marrow, with either autologous (self donated) or allogeneic (matching donor) stem cells. These are then re-infused into the patient. The hope is that new healthy cells will form and replace the diseased cells.
About The Author: Evamarie Hernandez, is a Senior Medical Laboratory Technology Student at Intellitec Medical Institute in Colorado Springs, Colorado, and an advanced Hematology student of Dr. Counce. Ms. Hernandez, an exceptional student, recently completed all didactic studies and is currently on externship. She will graduate with her Associates Degree in 2012. |
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