Category Archives: Blog Assignment 3

May
02
2013

Twith or Tic???

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Twitch or Tic???

Have you ever been sitting in class and all of a sudden your eye lid starts twitching? Well guess what? You could have a tic! Our book gives the example of our eyelids twitching as a tic! The definition is “a spasmodic twitching made involuntarily by muscles that are ordinarily under voluntary control”. So really, every time your eyelid twitches, it’s a tic. Don’t worry though, this does not mean you actually have tics. Tics are just a form of twitches.

WebMD.com tells us that most of the time twitches and tics are harmless, but on some occasions it may be a disorder. Tic disorders have repetitive and numerous twitches. They can actually be suppressed, but it can cause major discomfort to the person. It is not really known as to what causes tics, but lack of sleep and stress seem to play a role. Twitches, on the other hand, are what most people experience. These only happen on occasions and are completely involuntary. Extreme cases of eye twitches are called Blepharospasms, which can resemble an eye blinking tic. However, as stated earlier, the tic is controllable while the twitch is not. A twitch or a tic disorder does not usually cause a lot of problems in a person’s life style. They can, however, become disruptive and annoying.

A lot of people have the common eye twitch on occasion. It is nothing to worry about. However, if it becomes very repetitive, you may have a transient tic. Treatment for tics depends on how bad you have them. For transient tics, there is no treatment. You just have to learn to deal with them. On the bright side though, they only last for, at most, a year. For chronic cases that could lead to Tourette’s syndrome, doctors often prescribe medication to help settle the tics a little but mainly suggest behavioral therapy to teach patients how to cope with their disorder.

Tortora, Gerald J, Bryan Dickerson. Principles of Anatomy and Physiology. New York: Wiley, 2012. Print.

“Tic Disorders and Twitches.” Brain & Nervous System Health Center. WebMD, 03 Jan. 2012. Web. 02 Apr. 2013. <http://www.webmd.com/brain/tic-disorders-and_twitches?page=2>.

May
02
2013

Toads’ Leaping Legs

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Toads are generally known for their warts. However, the toad’s impressive attribute is its strong, powerful leg musculature. While the jumping distance is noteworthy, the landing ability is what is interesting to biologist Emanuel Azizi. The studies he performed involved the toad’s ability to protect its leg muscles by bracing for specific impact intensities.

When jumping, toads’ leg muscles contract. When landing, these muscles stretch. The body comes to a complete stop after moving at a fairly high speed due to the muscles acting as brakes. To disperse the energy and force of impact, the muscles of the legs take the risk of overstretching and possible injuries. A neuromuscular response to shorten the leg muscles that are involved in landing protects the muscles during larger impacts from jumping longer distances. How much the muscles shorten depends on the distance of the jump. The nervous system adapts the motor control patterns with each individual jump.

These findings can be applied to rehabilitation programs in the future. Neuromuscular deficiencies may be better understood by the looking at the strength and precision of the nervous system adaptations in toads. With further study into the sensory information being reported to the nervous system which enables the quick defensive measures to prevent injury, improvements can be made to the way we treat strains and overstretching injuries of muscles in humans.

References:

Nogrady, Bianca. “Toads Tweak Muscle Length to Soften Impact › News in Science (ABC Science).” Toads             Tweak Muscle Length to Soften Impact › News in Science (ABC Science). Australia’s Broadcasting              Company, 19 Dec. 2012. Web. 03 Apr. 2013.

University of California – Irvine. “Leaping toads reveal muscle-protecting mechanism.” ScienceDaily, 19  Dec. 2012. Web. 2 Apr. 2013.

Apr
25
2013

stem cell treatment for stoke

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Strokes are cerebrovascular accidents (cva) and are caused by lack of blood flow or blockage to the brain. People at risk of a stroke suffer from high cholesterol, high blood pressure and diabetes. Recent research has shown that stem cells can be used as cellular building blocks and can be administered to stoke patients and result in better recovery of brain function.

Stem cells are undifferentiated cells that divide through mitosis and can regenerate itself to make new cells. Stem cells are being used to cure diseases everyday. Patients receive stem cells intravenously or subcutaneously. The procedure seems to be very safe and promising, it only takes an hour, and has no known negative side effects. For safety precautions, the stem cells that are used go through extensive screening to check for imperfections. Fetal stem cells are used because the body does not reject them because they do not have a cellular fingerprint.

This unique treatment means that patients will not need more medications for their immune system. That helps their bodies be on less medication and save more money. There have been over 2000 men and women treated with these stem cells and the results of their treatments have been promising. There has been substantial improvements in all the patients. It takes patients 3 to 6 months to see any changes and improvements in their treatments.

 

Sources: J. Tortora, Gerald, and Bryan Derrickson. Principles of Anatomy and Physiology. 13th ed. John Wiley & Sons, Inc. Hoboken NJ, USA  2012.

“Breakthrough Stroke Treatment”. www.stemcellofamerica.© 2011 Stem Cell Of America

Apr
25
2013

Cystic Fibrosis

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Cystic fibrosis is a disease that causes mucous to be extra thick and sticky (Tortora, Derrickson 2011). Some organs in our body are lined with mucous. Cystic fibrosis affects the digestive and respiratory system. Breathing becomes difficult, out of the ordinary smelly bowel movements, constipation, lung infection, and stuffy nose are the symptoms that make everyday tasks harder than what they should be. The disease is inherited from one parent or both (Tortora , Derrickson 2011) . There are several ways to treat it, antibiotics and mucous thinners are a couple.

Speaking of Treatments, many people have found exercising have been a way to treat cystic fibrosis. The cardio workouts help the heart, which is a muscle, to become stronger. Recent studies have shown that people with cystic fibrosis who work out spend less time at hospitals paying for treatment (MediLexicon 2013). Also compared to a person with CF who does not work out, their growth and lung function has improved 21 % (MediLexicon 2013). Being active is a new treatment used to treat cystic fibrosis (MediLexicon 2013).

Exercising to treat Cystic Fibrosis is benefiting to the community because it is prolonging the life of our loved ones. Secondly it helps avoid paying for costly visits to the hospital and medicine. The hospitals may not benefit from the loss of revenue, but the money we spend there can be invested into our suffering economy and promote the growth of small work companies. Overall no one can lose. Life benefits all.

 

Literature Cited

  1. 1.    Tortora, Gerald J. Derrickson, Bryan H. Principles of Anatomy and Physiology. January 4th 2011

 

 

  1. 2.    Journal of Cystic Fibrosis. “Patients with Cystic Fibrosis Benefit from More Time At The Gym.” Medical News Today. MediLexicon, Intl., 1 Mar. 2013. Web.
    6 Apr. 2013. <http://www.medicalnewstoday.com/releases/257009.php>

 

Apr
25
2013

The Breathing Lung

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The Breathing Lung

            Thanks to a fascinating organ, called the lung, we are able to exchange oxygen and carbon dioxide with the blood, which allows our body’s cells to carry on their daily functions. However, there are people whose lungs no longer function properly and therefore need a lung transplant. A lung transplant involves surgically removing the lungs of a deceased person onto that of the recipient (1). Lung transplants can be performed from newborns to adults under the age of sixty five (1).

Usually once the donor lungs are removed from the cadaver they are placed inside an icebox where they are carried to the recipient (2). However, there is no longer any need for the icebox when one can have a breathing lung transplant instead, which the lung transplant team at Ronald UCLA medical have successfully performed (2). The devise, known as the Organ Care System (OSC), works by keeping the lungs alive and functioning while being transported (2). As soon as the lungs are placed in the device they are warmed and start breathing using oxygen and a supplementary solution of red blood cells (2). Dr. Abbas Ardehali, a professor and director at Ronald Reagan UCLA Medical Center, believes the breathing lung transplant device will not only allow them to improve the function of the donor lungs, it also makes it easier to access the donor lungs and carry them safely across longer distances (2). The OCS device is still going through clinical trials in lung transplant centers in Europe, Australia and Canada (2).

I believe the OCS device will have a positive effect on society. With this new technology device, the donor lungs will be tested before they are put into the recipient, which can determine if the donor lungs are adequate for the recipient; something that cannot be done in the iced box method. Also with the OCS device, the donor lungs can travel across longer distances and are safer than if they were on the iced box. Overall, not only will the OCS device help improve the lung transplant process, it will also save lives.

 

1.) “Lung Transplantation Procedure.” Johns Hopkins Medicine. The Johns Hopkins Hospital. Web. 27 Mar 2013.

2.) University of California, Los Angeles (UCLA), Health Sciences. “First ‘breathing Lung’ transplant in United States.” ScienceDaily, 26                               Nov. 2012. Web. 27 Mar. 2013.

 

Apr
25
2013

Tweaking Gene Expression to Repair Lungs

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Chronic obstructive pulmonary disease occurs when airflow to the lungs is blocked causing an increase of airway resistance (Tortorra and Derrickson). It is one of the highest causes of death of Americans and affects males more than females, but female COPD diagnoses have recently increased (Tortorra and Derrickson). Its primary cause is cigarette smoking or secondhand smoke meaning it can be prevented by avoiding those activities (Tortorra and Derrickson). There is no cure for COPD but there are available treatments to ease symptoms (ScienceDaily). However, recent studies have shown that with the use of epigenetics, chemical modifications to DNA and its proteins, can cause the lungs to regenerate damaged tissue and possibly curing the disease (ScienceDaily).

Dr. Ed Morrisey from the Institute for Regenerative Medicine in the University of Pennsylvania is researching the possibility of repairing the regenerative property of the lungs that is lost with pulmonary diseases (ScienceDaily). His studies show that a person with COPD had a lower amount of an enzyme called HDAC2 which he believes leads to the inability of the lung epithelium to regenerate properly (ScienceDaily). Further studies supported his belief when it was found that the different types of HDACs in the body functioned for both development and regeneration of lung tissue (ScienceDaily). With this finding, he believes that further studies of HDAC activity can lead to treatments that could potentially cure many types of lung diseases like COPD (ScienceDaily).

The lungs are one of the most important organs in the body and taking care of them is critical for an overall well being, and avoiding damaging such an important organ can prevent one from getting a lung disease. Respiratory diseases are all too common in America with millions diagnosed with Asthma, COPD, Emphysema, Chronic bronchitis, and other lung related diseases. These disorders are a big burden to those affected by them, and those with the disorder live the rest of their life with it as there are no cures only treatments for the symptoms. However, this recent study on the effects of the HDAC enzyme can lead to further research that could allow for a treatment with HDAC to regenerate damaged lung tissue that would cure many respiratory diseases.

Perelman School of Medicine at the University of Pennsylvania. “Tweaking gene expression to repair lungs.” ScienceDaily, 25 Feb.  2013. Web. 28 Mar. 2013

Tortora G.J. and B. Derrickson. 2012. Principles of Anatomy and Physiology. 13th ed., John Wiley and Sons

 

Apr
25
2013

Dendritic cells directly attack cancer cells

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Dendritic cells, which are derived from monocytes, are the most potent of the antigen-presenting cell types. They have long, branched projections that resemble the dendrites of a neuron, and they assist in the maturation process (Tortura & Derrickson). They play a role in anti tumor immunity because of their ability to acquire, process, and present to T lymphocytes tumor-derived antigens. There is current research being studied involving the correlation between various roles of dendritic cells and cancer treatment.

Research has show that dendritic cells can directly attack cancer cells and then present tumor antigens visible to T cells. Antigen presentation makes it easier for the immune system cells to recognize and attack cancer cells (Immunotherapy). Dendritic cells are immune cells that determine the type and regulate the strength and duration of T-cell responses. Also, they contribute to natural killer and natural killer T-cell anti tumor function and to B-cell-mediated immunity (PubMed).

The potential impact of the cytotoxic function of dendritic cells on their ability to present antigens has been a focus of intensive research. This examines the possible strategies to exploit the killing potential of dendritic cells in cancer immunotherapy (PubMed). By understanding the basic science behind the immune system, researchers will have more tools to combat disease and less people could suffer as a result.

Gerard J. Tortora and Bryan Derrickson. Principles of Anatomy and Physiology. 13th ed., John Wiley and Sons, 2012.

Hanke N, Alizadeh D, Katsanis E, Larmonier N (2013)

Dendritic cell tumor killing activity and its potential applications in cancer immunotherapy.

Immunotherapy. Cancer Vaccines. 25 March 2013. http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/immunotherapy/immunotherapy-cancer-vaccines

Dec
03
2012

muscular dystrophy by kaneshia morrow

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The subject I have chosen is “New Vitamin-Based Treatment That Could Reduce Muscle Degeneration” in relation to Muscular Dystrophy. Muscular dystrophy is a group of inherited muscle-destroying diseases that causes progressive degeneration of skeletal muscle fibers (Tortora). Many of us have experienced or have seen families that have a child with difficult walking or running. The disease does not just affect elderly men and women. The disease begins at a young age and can be genetically inherited.

Recently, research has been carried out by Clarissa Henry from the University Department of Biological Sciences at the University of Maine (PLOS Biology). As we all know, there is no cure to muscular dystrophy. Researchers have found ways to improve muscle functioning (in a zebrafish version) in muscular dystrophy by a cellular chemical called nicotinamide adenine dinucleotide which activates a cell adhesion pathway and prevents the normal junctions that are being formed among the cells in muscular tissue (PLOS Biology). The research has shown that zebrafish with muscular dystrophy have disorganized basement membranes in their muscular tissue which results in difficulties in movement.

I think that this is important research in relation to today’s society because the disease starts with the parents and runs down to their kids. The use of nicotinamide adenine dinucleotide can help prevent a person from having difficulties from walking, running and jumping. Taking this discovery seriously can decrease the number of people in the world being affected by muscular dystrophy. To conclude, it could possibly save the trouble that parents will go through when his or her child is suffering from muscular dystrophy by taking responsibility as a parent and taking vitamins that can decrease the chances that their child will develop muscular dystrophy.

Works Cited
Goody, M. F., Meghan, K. W., Reynolds, A. K., Crawford, B. D., & Henry, C. A. (2012, October 23). ScienceDaily: Muscular Dystrophy News. Science Daily: News & Articles in Science, Health, Environment & Technology. Retrieved November 8, 2012, from http://www.sciencedaily.com/news/health_medicine

Michelle F. Goody, Meghan W. Kelly, Christine J. Reynolds, Andre Khalil, Bryan D. Crawford, Clarissa A. Henry. NAD Biosynthesis Ameliorates a Zebrafish Model of Muscular Dystrophy. PLoS Biology, 2012; 10 (10): e1001409 DOI: 10.1371/journal.pbio.1001409

Tortora, Gerard J. and Bryan Derrickson. “Muscular Tissue.” Principles of Anatomy & Physiology. 13th ed. N.p.: John Wiley & Sons, 2012. 104. Print.

Dec
03
2012

Key Part of Old Mystery in Generating Muscle Mass Solved

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Muscle loss to disease and age is a widely studied subject because of the large population of elderly and the higher diagnosis of muscular disorders worldwide (Tortora and Derrickson 2012). Normally after 30 years of age humans begin losing muscle mass due to a variety of reasons such as decrease in exercise, and as a result of muscle mass loss: strength, muscle reflexes, and flexibility are affected (Tortora). According the article “Key Part of Old Mystery in Generating Muscle Mass Solved” from the ScienceDaily, Johns Hopkins researchers have identified how myostatin, a protein that muscle cells release to block further growth in the muscle, can be manipulated to increase muscle mass that would serve to help the elderly and patients who have been diagnosed with a muscular disorder (2012, September 27).Muscle stem cells, which serve to regenerate muscle mass when stimulated, known as satellite cells are affected with age and disease.

Knowing the effects of myostatin researches performed an experiment using specially bred mice to find out if myostatin binds to the satellite or muscle cells. Three tests where done in which the first group had defective satellite cells and the researchers blocked the activity of myostatin. They found that, blocking myostatin in the first group of mice resulted in an increase in their muscle mass suggesting myostatin did not act on satellite cells. A second experiment was performed with mice having functional satellite cells and the researchers again blocked myostatin activity. The results suggested that, although muscle mass increased in the absence of myostatin, the number of satellite cells did not, again suggesting myostatin did not affect the activity of satellite cells. Finally, to show that the relationship of myostatin is not with the satellite cells but with the muscle cells, researchers produced a group of mice whose muscle cells did not have the protein receptor that binds to myostatin. This experiment resulted in a notable muscle mass increase only in the mice whose muscle cells did not have the protein receptor that binds to myostatin, thus, establishing a meaningful relationship between myostatin and the muscle cell.

Because the cause of muscle loss and many muscular disorders affect satellite cells, focusing on the relationship between myostatin and the muscle cells could lead to better treatment for the elderly and those affected by muscle diseases. Although modern medicine has made a longer life possible, most who reach that stage of life deal with the pains and aches caused by muscle problems. So why not live a long life and live it for the most part comfortably? This lifestyle can be achieved by performing further research in the muscle cell and myostatin relationship.

Sources

Tortora G.J. and B. Derrickson. 2012. Principles of Anatomy and Physiology. 13th ed., John Wiley and Sons

Johns Hopkins Medicine (2012, September 27). Key part of old mystery in generating muscle mass solved. ScienceDaily. Retrieved November 25, 2012, from http://www.sciencedaily.com/releases/2012/09/120927141304.htm

 

Nov
26
2012

Muscular Dystrophy Blog

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Since we have been learning about muscles, I decided to write about muscular dystrophy. Muscular dystrophy is an inherited disorder. It involves degeneration of musculature that can get worse over time.  There are many different types of muscular dystrophy but they all have the obvious in common, the affect the muscles. However, some affect the upper body, some the lower body, and some the entire body. Also, in the different types, some muscles can be affected slowly and some quickly. Something not as obvious is that in some types of muscular dystrophy a symptom is mental retardation.

Duchenne Muscular Dystrophy is the branch of muscular dystrophy which mental retardation is common. Duchenne Muscular Dystrophy (DMD) is from a defect on the X chromosome and is more common in boys than girls. Mental retardation occurs in about thirty percent of the boys in which it affects. Along, with mental retardation DMD symptoms still include muscle weakness.

Unfortunately, muscular dystrophy is not an uncommon disease. Treatment is to control the symptoms because there is no cure for any of the variations of this illness. However, making more and more people aware of the disease is a goal. The more people involved in helping find a cure are making steps in the right direction. Once we find a cure it could help many people both young and old.

references

1.Kaneshiro, Neil K. “Muscular dystrophy.” U.S. National Library of Medicine – The World’s Largest Medical Library. A.D.A.M., Inc., 1 February 2012. Web. 7 November 2012. www.ncbi.nlm.nih.gov/pubmedhealth/PMT0002172/.

2. NARDES, Flávia; ARAUJO, Alexandra P. Q. C.  and  RIBEIRO, Márcia Gonçalves. Mental retardation in Duchenne muscular dystrophy. J. Pediatr. (Rio J.) [online]. 2012, vol.88, n.1 [cited  2012-11-23], pp. 6-16 . <http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0021-75572012000100003&lng=en&nrm=iso>.