G6d Essay

Parkinson disease (PD) is one of the most common neurologic disorders. and it affects approximately 1% of individuals older than 60 years old. Parkinson’s disease is a condition that progresses slowly by treatment. In addition, loss of pigmented dopaminergic neurons of the substantianigra pars compacta and the presence of Lewy bodies and Lewyneurites are the two major neuropathologic findings in Parkinson disease (Hauser, 2016).

It all started when Hahnemann first exposed the belief to himself with Peruvian bark. This caused symptoms of Malaria and it caused his body to adapt to the chills, fever and other symptoms that malaria would cause. He got excited for a while he only tested on himself but then moved on to do trials on his family. Also along the way he started to gain fans, a group of followers that were willing to let him test with them. The second treatment he wanted to find a cure for was small pox. He had no clue of how to do so, but he gave one thing a try. He injected small portions of cow pox to his wife. She began to get symptoms yes they were less severe but this gave him a chance to create a section of homeopathy for small pox, a huge breakthrough for medicine in this time. The bigger name medical schools and physicians did not support Hahnemann. They believe that his methods were not reliable and did not like that he could only put out one cure at a time and when he gave out the medicine he only did so in small portions to where they could not get the customers to pay high amounts limiting their

      Many of the doctors of the time were amazed at the horrible disease. Physicians were stumped about cure or even remedies of this illness. The only advice they could offer is to get away from it and start off new

The P1 cross was between four wmf females and nine wild-type males. The F1 progeny consisted of 12 wild-type females, and four triple-mutant males. The P2 cross resulted in 13 females, and 3 males, all with the wild-type phenotype (Table 1). The two parental crosses identify that the mutations are X-link recessive. The triple-mutant females of the P1 cross produce mutant male offspring, but wild-type females. The F1 females would be heterozygous for the mutations, but don’t express the mutations because they still have a wild-type X chromosome. However, the F1 males only have one X chromosome that comes from a mutant mother. The offspring for P1 were crossed again to make and F1 cross. The F1 cross would be X+/Y and X+/X. The F1 cross resulted in 100 F2 progenies over the course of 7 days.

Overall, the lack of dystrophin in DMD individuals causes many problems in different aspects of metabolism. It has a massive effect on muscles, affecting the shoulders, hips, calves, thighs, pelvic area first. Like other muscular dystrophies, DMD affects the voluntary muscles first and then will progress into other muscles. Limb-girdle muscular dystrophy is another type out of the many that affect voluntary muscles. Specifically, it targets the hips and shoulders.

The men involved in the experiment were told they were being treated for “bad blood”, a term used to describe syphilis, anemia and fatigue. They were under the impression that the doctors conducting the

In the case of diseases such as the DiGeorge syndrome, the immune system activity is not functioning properly due to the abnormal development of the thymus gland inducing a minimized production of T Cell. Whereas, in another case such as asthma, the immune system is overreacting. The other possibility of abnormality of the immune system is the impossibility for it to make a difference between invaders and the body’s cell causing the immune system to attack itself, those are the autoimmune diseases such as multiple sclerosis.1

Muscular dystrophy (MD) is a rare, progressive disease relating to the weakening of skeletal muscles. There are more than 30 types of muscular dystrophy that are further divided into nine categories. Duchenne MD is the most common and acute form of this condition that accounts for 50% of all the cases. Duchenne MD (DMD) is most prevalent in males, between the ages of 3 and 5 (Norwood, FL, et al. 2009). This X-linked disease occurs for 1 in every 3,500 males, which results in confinement to a wheelchair (Blake et al., 2002). Becker MD (BMD) is a less severe type of this condition. A study conducted in the United Kingdom by Bushby, Thambyayah and Gardner-Medwin, the incidence of Becker MD was estimated to be 1 in 18,450 males at birth

Gaucher disease (GD) is an inherited gene that stops glucocerebroside (type of lipid) to be broken down correctly. When this lipid cannot be broken down, buildups appear in the liver, spleen, and bone marrow which affects normal functioning. These organs begin to grow to an irregular size, amenia becomes present within the patient, and easy bruising appears due to the decrease in blood platelets. Gaucher disease is created during an autosomal recessive pattern, which means that two genes have a mutation, which causes the disorder. Normally, if a child is born with this disease, both parents carry one copy of the mutated gene. The gene that the mutation appears in is the GBA gene. GBA is located in chromosome one. The GBA gene is in charge of creating the instructions for producing an enzyme called beta-glucocerebrosidase. This enzyme breaks down the glucocerebroside into glucose and ceramide (a simpler fat molecule). When mutations appear in the GBA gene, the activity of the beta-glucocerebrosidase is reduced abundantly. Without this important breaking down of the

Classic Galactosemia, Type 1, is a complex disorder and the exact pathophysiology has is controversial. However, it is most commonly accepted that the main factor is the accumulation of galactose-1-phosphate, gal-1P, which is due to the impairment of galactose-1-phosphate uridylytransferase, GALT. This reaction uses the GALT enzyme as a part of the Leloir pathway which enables the body to process galactose.

The reading shows disease and inheritance in an entirely new light. It introduces the idea that genetically inherited diseases may have been selected for, which means that they must provide certain evolutionary advantages. It reorients the reader’s perspective about a disease like hemochromatosis, which has the potential to be incredibly harmful and even deadly, establishing that it may have once provided protection from the bubonic plague, making it an advantageous trait. This brings other genetic diseases into question, examining why diseases that appear to be harmful have not been eliminated from the gene pool. The idea that a disease that is harmful and dangerous in modern times could have once been a beneficial adaptation is very interesting.

The focal point of this journal article focused on how the inherited genetic disease; Sickle cell anemia, is influenced by ethnicity and ancestry; two key categories that must be considered when explaining genetic associations and comparing traits amongst a population. This article compared the genetic profiles of African Americans with sickle cell disease to individuals of the Caucasian/ European descent and African descent. They discovered that although there is slight genetic comparison between ethnicity, there are more similarity in relation to ancestry and the Sickle cell trait. Three ancestry’s that resonated the most were the Mandinka’s, Yoruba’s, and Bantu from West Africa. In this study, researchers combined genome data from different

Hutchinson-Gilford progeria syndrome is a very rare genetic disorder that causes the affected individuals to appear older than what they are. Individuals are able to be affected by this disorder as earlier as a their first few months of life. There have been reported cases of infection seen in the fetus. Characteristics of progeria include limited growth such as short stature and low body weight, full body hair loss, and facial features that resemble an aged person. This genetic disorder can lead to other health complications such as degeneration of bone mass and tissue, scleroderma, kidney failure, loss of eye sight, atherosclerosis, and severe cardiovascular problems. There is a genetic test to diagnosis the disorder at a younger age called HGPS. Currently, there is no cure or treatment for the disease. However, patients can undergo certain surgeries such as

The experiments in the 1800s revealed the mystery of the Calabar beans and its physiochemical properties. In the 1855, Robert Christison, a Scottish toxicologist and physician experimented Calabar bean on himself. When he realized he poisoned himself, he drank soapy water to make himself vomit. In the 1862 Thomas Fraser found the power of physostigmine contracting the pupils of the eyes. In the 1864, the alkaloid was crytallized by Jobst and Hesse, which they called “Physostigmine”. In the 1865, Vee and Leven independently isolated an alkaloid from Calabar beans. They called it eserine. In the 1870, the Calabar beans were used successfully to treat glaucoma. In the 1973, Barthlow discovered the antagonism between atropine and physostigmine. In the 1935, Percy Julian accomplished the first total synthesis of the physostigmine. In the 1936, Ed Alburquerque discovered that physostigmine protects against nerve gases.

caused ulcers. It was backed up by Weiner et al in 1957. He used army