Knee jerk reflex perfect paragraph

Submitted by koganezova on Fri, 03/24/2017 - 12:23

The muscle stretch reflex is an automatic response our skeletal muscle goes through when it is stretched. Once the skeletal muscle is stretched, there is a reflex that wants to bring the muscle back to contraction. This is thought to hold a protective purpose. This is how the knee jerk reflex comes in. When the doctor hits your knee with the hammer, he hits your tendon which in turn causes your thigh muscle to stretch a little bit. Shown through the muscle stretch reflex, once that thigh muscle stretches even a little, the reflex causes the muscle to contract which in turn kicks your leg up. 

Lung Cancer

Submitted by seszlari on Fri, 03/24/2017 - 12:13

Today, lung caner is the leading cause of cancer death in the world. More than 300,000 Americans today have already been diagnosed with lung cancer. This cancer is found mostly in the elderly for the majority of people with lung cancer are over the age of 60. However lung cancer is the leading cancer that causes death in both men and women in the United Sates of all ages. An estimated 158,040 Americans are predicted to die from lung cancer in 2015, roughly 27 percent of all cancer deaths.  

 

Auditory System Perfect Paragraph

Submitted by matjbaker on Fri, 03/24/2017 - 11:46

     The pressure wave enters our ears through the outer ear and proceeds to interact with the tympanic membrane, also known as the ear drum. At the ear drum, the pressure wave is converted to vibration that is passed from the tympanic membrane to small bones in the ear known as ossicles. The ossicles act as a lever and pass the force along to the oval window. The ossicles are able to act like a lever because of the difference in surface area between the tympanic membrane and the oval window. The same amount of force applied over a smaller surface area results in greater pressure and allows for amplification of the signal.

NeuroBio Write Up #2

Submitted by dkotorobay on Fri, 03/24/2017 - 11:46

Title: Red-shifted channelrhodopsin stimulation restores light responses in blind mice, macaque retina, and human retina

Main Points:

The question the paper is trying to answer is whether or not using red-shifted channelrhodopsin to treat degenerative blindness will work as it did in mice.

This study is important because it could possibly be a way to treat vision loss caused by retinal degeneration.

The results were that red-shifted channelrhodopsin also drives neuronal responses in macaque retinae as well as in the central human retina, the site of high-acuity vision, demonstrating the therapeutic potential of the red-shifted channelrhodopsin molecule.

Methods:

The models used were rd1 mice, macaque retinal explants and humans.

The techniques:

For the blind mice AAV2 injections through the sclera.

For the primates they were terminally anesthetized and their eyes were removed and the retina was isolated from the vitreous humor and cut into 1 cm pieces. The retinal explants were infected with the AAV2 and AAV8 until the day of electrophysiological recordings or fixation, the AAV infections were performed within 2 hours of the retina explants being put in tissue culture.

 For the human experiments postmortem human ocular globes were acquired from the school of surgery, 6 donors, 63 – 95 years old, postmortem delays 9 – 38 hours. Similar proceedings to the primate experiment.

Shortcomings/Weaknesses:

The age range constrained to older ages in humans, the pool of human subjects was small, only 6 people. There were also no live subjects after the mice. This may be an ethical issue.

The controls were appropriate, they tested multiple models in the same manner, though the mice were alive and the primates and humans were not alive.

Figures:

Figure 1: 3 panels, showing that the channelrhodopsin can be efficiently targeted to the RGC membrane and dendritic arbor of blind mice.

Figure 2: Graphs showing the responses triggered by optogenetic stimulation of the retina.

Figure 3: Different types of graphs showing the triggered responses in the blind mice that were treated with the AAV2.

Figure 4: One of the figures shows the locomotive behavior of the blind mice before and after treatment as well as graphs that correspond with those results.

Figure 5: Graphs showing the light responses in the AAV-infected primate retinae.

Figure 6: I believe these graphs and pictures are demonstrating where and what is activated when the explant has been infected with the AAV.

Figure 7: Pictures of the retina showing part of the foveal pit.

Figure 8: AAV- mediated optogenetic activation of the human retina after it had been incubated for 12 days.

Questions:

How would such an experiment work on a live human? Would it be conducted more like the mouse experiment?

Keywords:

Treating degenerative blindness, channelrhodopsin used to treat vision loss

Nervous System Journal Entry

Submitted by maurabenson on Fri, 03/24/2017 - 11:26

The neuron is a highly specialized cell responsible for communicating with the rest of the body using electrical and chemical signals. Thye are compposed of many parts. The dendrites are appendages that receive information from other neurons. The soma is the cell body of the neuron that contains the nucleus, the ribosomes and other organelles. The nerve receives either excitatory or inhibitory impulses and when the signal reaches the axon hillock, an action potential is fired down the axon, which sends signals to other neurons. The nerve terminal is at the very end of the axon where the neurotransmitters are released. The nerve terminal is also part of the synapse, which contains the nerve terminal of the presynaptic neuron, the membrane of the postsynaptic neuron and the space between them, which is the synaptic cleft. The axons of neurons are insulated by myelin which is either produced by oligodendrytes in the central nervous systema or by the Schwann cells in the peripheral nervous system. Besides neurons, there are helper cells in the nervous system which are called glial cells or neuroglia. These include astorcytes which nourish the neurons and create the blood brain barrier and  epidymal cells which line the ventricles and create cerebrospinal fluid. Microglia are phagocytes that work in the nevous system and the schwann cells and oligoendrytes also fall into this category. 

The ability for a neuron to communicate with other cells depends on the membrane potential of the cell. The resting membrane potential which is when the cell is at equilibrium is -70mV. This is upheld by a Na/K ATPase which pumps 3 sodium out of the cell while bringing 2 potassium in. The signals that the cell recevies either makes the inside of the cell more positive, is an excitatory signal while the signals that make the inside of the cell more negative are inhibitory. Neurons are constantly receiving signals and the sum of the signals determines whether or not an action potential is fired. This is called summation. When the signal is strong enough to cause an action potential, the signal reaches the axon hillock which opens up voltage gated sodium channels allowing sodium to flood into the cell causing the cell to depolarize. When the cell reaches 35 mV, the the sodium channels close and the potassium channels open causing the cell to depolarize. 

Mammalogy Notes Part 1

Submitted by dkotorobay on Fri, 03/24/2017 - 11:05

Ungulates: mammals with hooves. Claws, nails, and hooves: unguis- keratinized. subunguis- transition to skin. pad- skin (may be sensitive). There are two orders of ungulates: order Perissodactyla: odd-toes ungulates, order Artiodactyla: even-toed ungulates. Order Perissodactyla: mesaxonic foot, order Artiodactyla: paraxonic foot. (the astragalus is called the talus in humans). Convergent adaptations for cursoriatlity (running): the development of the astragalus as the main weight bearing bone (the calcaneus in humans), reduction/fusion of the metapodials into a cannon bone. The shape of the astragalus in perissodactyls and artiodactyls: O. Perissodactyla: top surface pulley-shaped, bottom surface is flat. Limits movement between the leg and ankle to flexion and extension. Less mobility between ankle and foot, limits movement to flexion and extension. Shared derived characteristics: enlarged astragalus with pulley-shaped upper surface only, mesaxonic feet with a reduction of digits, all are hindgut fermenters (enlarged caecum with commensal bacteria). Family: Tapiridae- tapirs (Tapirus): they are morphologically primitive: unspecialized limbs, primitive tooth number (44), simple loph pattern to teeth (like rhinos). They have: reduced nasal bones, elongated proboscis formed by nose and upper lip. They generally live near swamps, rivers or other wet areas where they eat succulent plant material and fruit, all are either endangered or vulnerable, all pops. are decreasing. Family: Rhinocerotidae: Live in a variety of habitats but need permanent water, prefer to eat leaves and grass but will eat woody vegetation and fruit. Diceros bicornis (black African and Asian rhinos): pointed, prehensile upper lip for browsing. Ceratotherium simum (white African rhino): square lip for cropping grasses (grazing). Behavior: solitary or mom/offspring groups, females breed at 5/6 years, males at 10, usually a baby every 2-4 years. Horns: mass of long hair-like fibers fused together, composed of mineralized keratin with no bony core or sheath. Family: Equidae: the most cursorial perissodactyl: calcaneum is long and posteriorly placed, astragalus is weight-bearing, foot greatly elongated, only 3rd digit is functional. All equids are grazers. Behavior: polygynous (1 male, many females), strong social hierarchy- led by single stallion., herds based on extended family groups/ “clans”, social structure regulated by complex behaviors and vocalizations. The development of grasslands in the early Miocene is thought to be the driving force behind the evolution of horses. Were highly diverse in the past, Baluchitherium (Peracetatherium), from the Oligocene of Pakistan, is the largest known land mammal. Megacerops (Brontops) was the equivalent of a forest elephant in the late Eocene of N. America. 

Ethics

Submitted by scestero on Fri, 03/24/2017 - 10:36

Since the Human Genome Project was finished in 2005, there have been an array of both benefits and issues that have arised in the field of genetics. As genetic testing is becoming more readily available, more and more people are getting tested for various ailments that are related to genetics. What people forget to understand is that just because you have the gene, it doesn't mean that it will be expressed or that you will that particular disease. For example, having cancer alleles doesn't mean you will have cancer, but having the Huntington's allele does mean you will have Huntington's. In 2015, president Obama issued a Genetic Discrimination bill. This bill prevented employers and insurance companies from denying people who have undergone genetic testing and have ay ailment. This became a huge problem because insurance companies refused to cover individuals with cancer associated alleles for cancer. This poses a major problem in the field of ethics and medicine. Do you think people should be covered for ailments found in their genetic code.

epigenetic pp

Submitted by jdantonio on Fri, 03/24/2017 - 10:32

Epigenetic modification is associated with the inheritance of many different genetic disorders, two of which are angelman syndrome (AS) and prader willi syndrome (PWS). Two closely related genes that are associated with maternal and paternal line genetic imprinting, a type of epigenetic modification, and de novo deletions cause these disorders. In PWS the gene that creates the functional gene product is imprinted in the maternally inherited mammalian chromosome, this is usually compensated for by the presence of the functional gene in the paternal chromosome. PWS is caused by a de novo deletion of the paternal copy of the PWS gene, coupled with its maternal imprinting this causes the individual who inherits these chromosomes to have no active functional copy of the PWS gene and thus causes PWS. The AS gene is conversely imprinted in the paternal chromosome of mammals and is compensated for by the expression of the AS gene in the maternal chromosome. In AS the AS gene has been lost on the maternal chromosome by a de novo deletion of the AS gene. With the paternal copy of AS inactive do to imprinting and the maternal copy of AS lost to deletion, no functional copy of AS is present and the AS disease phenotype occurs. These genes are said to be sister diseases as their inheritance is mirrored, one caused by paternal imprinting and maternal deletion the other by maternal imprinting and paternal deletion, and they are located in the same region of the chromosome. Together AS and PWS provide an excellent example of epigenetic effects on trait inheritance. 

King Snake Perfect Paragraph

Submitted by amprovost on Fri, 03/24/2017 - 10:29

     A recent study compared the constricting power of both king snakes and rat snakes, two different kinds of snake who kill their pray by way of constriction. It was shown that king snakes produce twice the constricting power of rat snakes per square inch, despite having very similar levels of muscle mass. This test was conducted by putting pressure sensors in the body of a dead mouse and shaking it in front of these snakes, causing them to constrict said mouse like it was living prey. This revelation seems to indicate that a snake's power comes not from its muscle system but rather from how it orients its body. This discovery has laid the groundwork for futher studies into the topic, perhaps allowing researchers to discover more about how constrictors work.

 

Ethics

Submitted by scestero on Fri, 03/24/2017 - 10:23

In todays world we can do an array of things with genetics and medicine, ever since the human genome prject was finished. In 2015 president Obama issued a bill saying that employers and insurance companies are not allowed to not hire you due to genetic test results. Many insurance companies won't cover people who have gotten genetic testing and come out with a cancer allele, Huntingtons or diabetes. If they do cover these people they wont cover the specific diseases that have been found in your DNA. The law was passed because employers and insurance companies were looking at peoples private genetic testing results. The problem with this is that with most of these ailments you are not definetely going to get them if you have the allele. 

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