My research interests lie in cell signaling, and more broadly, in sensory processing. My interest

When I first entered college, I had thought that I wanted to major in Biomedical Sciences. The reason being, I was diagnosed at the age of 7 with Type 1 Diabetes. I was tossing around the thought that I was interested, possibly, in having a career that involved my disease in it. From being a part of this compass program, I have learned about many careers. Even though I learned more of what I do not want to do, it has helped me narrow down to majors that I am more interested in. I was thinking of still having the possibility of entering the medical field, but I am unsure. Learning about the different careers in the medical field and visiting labs has shown me that it isn't something that I am interested as much as when I first enter college. While I do want to be involved with my disease, I’m not sure if I want to have a career with it, but it could still be a possibility.

1. Describe the basic functioning of a neuron beginning with receiving signals from other neurons or sense organs and ending with the transmission of a signal to another neuron. Explain how a pattern of neuron firing is related to behavior.

The nematode Caenorhabditis elegans has ended up being a capable model for the investigation of maturing science. Strikingly, C. elegans tissues fall apart at various rates in maturing grown-ups, with specific highlights of age-related decrease strikingly reminiscent of those in higher life forms. Here they report two striking highlights of the maturing C. elegans sensory system—auxiliary regrowth and synaptic weakening. Morphological changes that happen amid maturing are neuron-particular and incorporate new dendrite outgrowth from forms or somata, with mitochondria regularly arranged at the branch point for the new neurite. Since morphological expanding or growing and synaptic decrease without cell passing exemplifies maturing human mind, enter factors in age-related neuronal decay might be preserved crosswise over phyla.

After a retinal molecule absorbs light, the normally 11-cis form of the bound retinal molecule straightens to become the 11-trans from. This change activated the opsin molecule. Opsin activates transducin which is a G protein. This G protein then activates phosphodiesterase. Phosphodiesterase is an enzyme that breaks down cyclic-GMP. The break-down of cyclic-GMP removes them from the gated sodium channels and makes the gated sodium channels inactive. Because of this, sodium ion entry into the cytoplasm decreases.

In this project, C. Elegans are hermaphrodite worms that will be used since they are easy to maintain in lab, as well as have short life cycles. The gene that the project attempted to knockdown in C. Elegans with RNAi treatment is the unc-22 gene. RNAi disrupts gene expression in the presence of double stranded RNA (dsRNA) that is complementary to target gene sequence. The unc-22 gene codes for a muscle protein called twitchin in wild-type worms. The Unc-22 is required for muscle regulation and maintenance in C.Elegans. To verify that the RNAi treatment worked, would check the unc-22 mRNA levels in the worms, in addition to phenotype observation.

Many sporadic melanomas are also found to have mutations or loss of expression of this tumor suppressor gene, known to act in the same signaling pathway as the retinoblasma cases (see 3.3 Tumor suppressor genes).

Retinitis pigmentosa is a group of inheritable diseases that is characterized by gradual deterioration of the photoreceptors in the retina. The photoreceptor cells in the retina, rod cells, are light sensitive cells that are able to sense low levels of light. The frequency of retinitis pigmentosa is one in four thousand births (Deng et al., 2015; Fahim et al., 2012; Haddad et al., 2016; Shu et al., 2012) People affected by retinitis pigmentosa will typically exhibit symptoms of night-blindness first, and this will precede a loss in the patient’s visual acuity field that starts from the outer edge and gradually moves inward resulting in a much smaller visual field and loss of peripheral vision, also known as tunnel vision (Haddad et al., 2016).

Neurodegenerative diseases continue to affect the lives of millions Americans each year, with incidence and prevalence rates ever increasing. These diseases cause degeneration or death of nerve cells in the brain. These diseases can cause a financial and emotional burden on not only patients themselves, but also family members and care givers as well. Molecular mechanisms that underlie these diseases have remained relatively unclear, despite much research. Understanding the mechanisms of these diseases are facilitated by utilizing model organisms to study pathways involved in neurodegenerative diseases. One such model organism is the Caenorhabditis elegans nematode. The C. elegans roundworm has displayed usefulness as a template to study neurodegenerative diseases in humans, including Parkinson’s disease and Alzheimer’s disease.

Strikingly, C. eleganstissues fall apart at various rates in maturing grown-ups, with specific highlights of age-related decrease strikingly reminiscent of those in higher life forms. Here we report two striking highlights of the maturing C. elegans sensory system—auxiliary regrowth and synaptic weakening. Morphological changes that happen amid maturing are neuron-particular and incorporate new dendrite outgrowth from forms or somata, with mitochondria regularly arranged at the branch point for the new neurite. Since morphological expanding/growing and synaptic decrease without cell passing exemplifies maturing human mind, enter factors in age-related neuronal decay might be preserved crosswise over phyla.

Malignant melanoma is the most commonly seen skin cancer and it has the highest number of deaths among diseases of the skin (Friedman, Rigel, Kopf and Polsky, 2005). Among the many factors that cause this cutaneous cancer genetic modifications, viruses, carcinogens and excessive exposure to ultraviolet rays are the most commonly occurring (Friedman, Rigel, Kopf and Polsky, 2005). Malignant melanoma affects all areas of the skin and the disease forms in melanocytes, which are the cells in which pigments (melanin) are synthesized (Melanoma Treatment). The cancer has its origin in the epidermis and affect squamous and basal cells. The disease usually affects the trunk, arms and legs but can also be present in the eye, affecting the

While researching in depth Ocular Melanoma, there has been a consistent theme persisting there is not enough research done to find a way to decrease metastasis percentage and increase survival rate. The current attempts at decreasing metastasis and increasing survival rate have stayed the same throughout the course of 4 decades. The current drug, LS2616, is being used to treat Ocular Melanoma patients, but it is used to late to feel the full impact of the drug. Research and Development laboratories are working on a faster-acting drug, but nothing has been tested on mice or released to the public. If new drugs could be created, the survival rate of Ocular Melanoma would increase drastically.

For AP Biology I chose cell signaling because I had worked with a friend to complete this assignment. We needed to remain curious in

Enhance the affinity of the recognition site for GABA by inducing conformational changes that make GABA binding more efficacious.

The physiological function of each receptor subtype has not been established and is currently the subject of intensive investigation (1).

Three other genes make proteins that are also involved in melanin pigment formation and albinism, but the exact role of these proteins remains unknown. These genes are the P gene on chromosome 15, the Hermansky--Pudlak syndrome gene on chromosome 10, and the ocular albinism gene on the X chromosome.