Cerebral Spinal Fluid (CSF ) is produced by the ependymal cells in the choroid plexus in the brain and its main purpose is to absorb shock and provide protection to the brain. CSF flows between the pia mater and arachnoid mater of the brain and is reabsorbed through the arachnoid villi. If CSF is not formed or drained, hydrocephalus occurs.

Hydrocephalus is an abnormal buildup of CSF in the brain cavities (often called “Water on the Brain”) (1). Hydrocephalus occurs when there is an obstruction in the brain that prevents the proper drainage of CSF (1). The buildup of CSF causes an increase of pressure inside the skull, which in turn, inflicts pressure on the brain (1). Hydrocephalus can be caused by congenital abnormalities, head injury, and meningitis (3). Symptoms of hydrocephalus vary depending on age, the level of progression, and individual tolerance of the disease (2). Some typical symptoms for hydrocephalus includes: problems with walking, impaired bladder control, mental impairment, and dementia (2). The effects of hydrocephalus can be life threatening (1). If left untreated, convulsions, head enlargement, brain damage, and death can occur (1).

Hydrocephalus is a very serious condition and is highly significant to treat after receiving an injury to the head and/or noticing some of the symptoms mentioned above. If left untreated, a person could not only be forced to endure the pain of an enlarged head due to the buildup of fluid that was meant to protect the most vital organ in the body but might possibly die all because they failed to treat their hydrocephalus condition.

1. Nordqvist, Christan.  “What Is Hydrocephalus(Water On The Brain)? What Causes Hydrocephalus?” MNT. 10 Mar. 2010. 16 Nov. 2012 < http:// www .medicalnewstoday .com /articles/181727.php>
2. “Hydrocephalus (cont.).” MedicineNet.com. 16 Feb. 2011. 28 Nov. 2012 http://www. medicinenet.com/hydrocephalus/page3.htm
3. Tortora, Gerald J, Bryan Dickerson. Principles of Anatomy and Physiology. 2009.

Hydrocephalus actually means water on the brain. It is a buildup of cerebrospinal fluid in the skull that leads to brain swelling. Hydrocephalus can occur in adults and the elderly, but it’s most common in children. Buildup causes an abnormal stretching of the ventricles and puts abnormal pressure on the brain (Tortora 502).

University of Iowa researchers have discovered that defects in certain cells, which are important to brain development, are linked to hydrocephalus. Hydrocephalus has been treated by brain surgery to remove excess fluids for about 50 years. The University of Iowa researchers have studied immature mouse cells known as precursor cells. These cells play an important part in brain development. The team discovered an imbalance in the process of immature cells growing then dying off which eventually caused hydrocephalus. The team treated the mice with lithium and noticed the cells turning back to normal (Sines).

Three out of every one thousand babies are born with some type of hydrocephalus. Since brain surgeries were used to treat hydrocephalus, this new discovery could reduce the time it takes to heal from the treatment. This discovery can improve the lives of many children, adults, and elderly. This new technique can be the start of treating many more diseases.

Sines, Vonda. “Hydrocephalus Linked to Cell Flaws in Brain Development.” www.news.yahoo.com. N.p., 20 2012. Web. 29 Nov 2012.

Tortora, Gerald J, Bryan Dickerson. Principles of Anatomy and Physiology. 2009.

New research in the link between migraines and dementia or cognitive decline suggest that one is not associated with the other. Migraines result in sharp pain in one side of the brain and is accompanied with other symptoms such as nausea, vomiting, and sensitivity to light and sound (Mayo Clinic). Worldwide, twenty percent of females are affected by migraines, but a new research from Brigham and Women’s Hospital has suggested that migraines do not have the long term consequences commonly associated with it (ScienceDaily).

The Women’s Health Study, which consisted of about 40,000 women from ages 45 and older, was used to test the relationship between migraines and cognitive decline. Four groups were created: one with no history of migraines, migraines with aura, migraines without aura, and past history of migraine (ScienceDaily). Migraines with aura are those that include the normal symptoms but also with flashes of light, blind spots, or tingling in arm or leg prior to the onset of the migraine (Mayo Clinic). The study was carried out in a two year interval with up to three cognitive test at a time. The results were that women with no past history of migraines and those that did had no significant cognitive decline differences (ScienceDaily).

Cognitive decline which affects memory retention can negatively impact one’s daily life, but seeing that there isn’t a significant link between migraines and cognitive decline can bring hope to those that experience them. This study can help doctors in better diagnosing their patients since migraines are normally associated with cognitive decline, and cognitive decline is the first step to Alzheimer’s, which affect about 11% of those over the age of 65 (Tortora and Derrickson 2012). Further research in the affects of migraines will eliminate older beliefs about it and result in better treatment to the large population that are affected by migraines today.

Sources

Brigham and Women’s Hospital. “Good news. Migraines hurt your head but not your brain.” ScienceDaily. 10 Aug. 2012. Web. 29 Nov. 2012

Mayo Clinic Staff. Migraine. http://www.mayoclinic.com/health/migraine-headache/DS00120. Accessed November 29, 2012.

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

Every 45 seconds, someone suffers a stroke in the United States. Each year, 1.7 million people suffer a traumatic brain injury (TBI) in the United States.  A stroke results from an artery bursting, leaking, or becoming obstructed, which deprives the brain of oxygen and leads to cell death. A traumatic brain injury results from a blow to the head or a penetrating brain injury that disturbs the brain’s normal functions. Fortunately, a medical breakthrough has been made that may restore some brain function, even if years have gone by since the stroke or traumatic event.

Researchers at the Institute of Neurological Recovery (INR) discovered that one dose of etanercept can quickly improve neurological problems caused by a stroke or traumatic brain injury. Etanercept works by binding to and deactivating an immune molecule that is responsible for excessive brain inflammation. An observational study conducted involving 629 patients demonstrated the potency of this claim. Most of the patients experienced significantly rapid improvement in cognition, motor impairment, and spasticity, after receiving a dose of etanercept. The study was carried out long after spontaneous meaningful recovery would be likely.

In the years to come, this groundbreaking discovery may have a dramatic impact. People left severely debilitated after suffering a stroke or traumatic brain injury may finally be able to resume their normal lives. Also, countless lives may be spared, if a person receives a dose of etanercept, before the damage progresses too far.  People from all around the world, not just the United States, may greatly benefit from this medical discovery.

Sources:

J. Tortora, Gerald, and Bryan Derrickson. Principles of Anatomy and Physiology. 13th ed. John Wiley & Sons, Inc. Hoboken NJ, USA  2012. Page 553. Print.

“New Breakthrough for Treatment of Traumatic Brain Injury and Stroke.” Institute of Neurological Recovery. Institute of Neurological Recovery. 31 Oct 2012. Web. 29 Nov 2012.

Neurons are the fundamental cell of the nervous system which directs responses to stimuli, coordinates activities of other organ systems, and interprets sensory information about external conditions (Tortora and Derrickson 2012).  These neurons send information from neuron to neuron through synapses by electrical or chemical signals.  Scientists are studying how neurons do not need to synapse with other neurons to be able to send and receive information.   Neuron communications are being observed to take place without any direct connections to other neurons.

Jean-Pierre Rospars was the first to observe what is called ephaptic interactions in flies, which occurs when a neuron silences a neighboring neuron instead of sending the signal though the nervous system.  Studies by Chih Ying-Su, on Drosophila melanogaster were completed by a test on two neurons (ab3A and ab3B) which control for methyl hexanoate and 2-heptanone, respectively.  After being exposed to each of the chemicals individually, the exposed neuron would spike while the other neuron would be shut down.  This is the example of ephaptic interactions Su was looking to expose.

Su also tested these interactions by introducing synaptic blocking chemicals to Drosophila melanogaster.  The test was completed between two neurons that dealt with the flies attraction to apple cider vinegar and the distaste for carbon dioxide.  After blocking the synapses for vinegar, the flies were placed in front of two arms which both contained carbon dioxide, but only one arm also enclosed vinegar.  The flies followed down the arm with the added vinegar which gave Su a conclusion that flies were using fluid inside of the sensillum to create an electric field when the neuron was being blocked.

The phenomenon known as emphatic coupling has been discussed for a long time but it has been perceived as obscure.  A factor in the arcane observations has been the lack of evidence on the subject.  Further studies, along with the study completed by Su, show that knowledge of this occurrence might be useful for protecting crops from hungry insects, or people from disease-carrying insects.

Sources:

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

Su, Chih-Ying; Menuz, Karen; Reisert, Johannes; Carlson, John R. “Non-synaptic inhibition between grouped neurons in an olfactory circuit.” Nature. 21 Nov. 2012. <http://www.nature.com /nature/journa/vaop/ncurrent/full/nature11712.html?WT.ec_id=NATURE-20121122

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.

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