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My Name is Jim.

My Name Is Jim - Synopsis

“So I graduated from writing, how did I get here?” The film opens up with protagonist, Jim, beating into his first victim, David. We learn that Jim is a debt collector trying to collect from his victims to pay off his sister’s debt to the loan sharks. Back home, Jim tries to write a novel but can’t seem to come up with an idea. Jim has a complicated relationship with his sister, Dianne as she’s often the one who takes care of the place through his sarcastic remarks. As soon as Dianne leaves for college, Jim calls up his best friend, Kavin, out for mamak.

Over their conversation, Jim tells Kavin that he’s broke and is soon recommended to take up a part time job to cover his expenses. Jim tries to apply for a job as a barista only to have his offer declined by the manager of the store himself. Jim spots his sister from afar and is troubled by this. He gets a call from Don and has to explain that he doesn’t have the money yet. He makes a promise to Don that he will get the money soon then heads off to find David once more. Much later, David is preparing to leave his apartment when Jim awaits him outside.

“You going somewhere?” David denies this as Jim asks him about the money. David exits the dorm and takes their conversation away from the apartment. They talk and find out more about each other but Jim seems almost unfazed by his explanation. They struggle at the edge of the apartment for the money only to have David die. Jim comes home much later in the night to explain to Dianne about what happened that night. Dianne finally reveals why she borrowed the money in the first place, telling him off for being too lazy to do anything.

The next day, Dianne leaves home again, it’s unclear what her intentions are but what she had told Jim struck him with an idea. He calls Don and tells her that he has her money. Jim waits for Don at a café patiently and when she arrives, it isn’t as he’d expect. He tries to negotiate with Don on their new terms only to have it nonchalantly agreed upon. She takes the package and leaves, having Jim just sit there, contemplating his life beyond this. He realizes that now, he is put into a loop of constantly collecting. He is a debt collector.

Final Script

Fairy Disease research

Description

Fabry disease is an inherited disorder that results from the buildup of a particular type of fat, called globotriaosylceramide, in the body's cells. Beginning in childhood, this buildup causes signs and symptoms that affect many parts of the body. Characteristic features of Fabry disease include episodes of pain, particularly in the hands and feet (acroparesthesias); clusters of small, dark red spots on the skin called angiokeratomas; a decreased ability to sweat (hypohidrosis); cloudiness of the front part of the eye (corneal opacity); problems with the gastrointestinal system; ringing in the ears (tinnitus); and hearing loss. Fabry disease also involves potentially life-threatening complications such as progressive kidney damage, heart attack, and stroke. Some affected individuals have milder forms of the disorder that appear later in life and affect only the heart or kidneys.

Frequency

Fabry disease affects an estimated 1 in 40,000 to 60,000 males. This disorder also occurs in females, although the prevalence is unknown. Milder, late-onset forms of the disorder are probably more common than the classic, severe form.

Genetic Changes

Fabry disease is caused by mutations in the GLA gene. This gene provides instructions for making an enzyme called alpha-galactosidase A. This enzyme is active in lysosomes, which are structures that serve as recycling centers within cells. Alpha-galactosidase A normally breaks down a fatty substance called globotriaosylceramide. Mutations in the GLA gene alter the structure and function of the enzyme, preventing it from breaking down this substance effectively. As a result, globotriaosylceramide builds up in cells throughout the body, particularly cells lining blood vessels in the skin and cells in the kidneys, heart, and nervous system. The progressive accumulation of this substance damages cells, leading to the varied signs and symptoms of Fabry disease.

GLA gene mutations that result in an absence of alpha-galactosidase A activity lead to the classic, severe form of Fabry disease. Mutations that decrease but do not eliminate the enzyme's activity usually cause the milder, late-onset forms of Fabry disease that affect only the heart or kidneys.

Inheritance Pattern

This condition is inherited in an X-linked pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes in each cell. In males (who have only one X chromosome), one altered copy of the GLA gene in each cell is sufficient to cause the condition. Because females have two copies of the X chromosome, one altered copy of the gene in each cell usually leads to less severe symptoms in females than in males, or rarely may cause any symptoms at all.

Unlike other X-linked disorders, Fabry disease causes significant medical problems in many females who have one altered copy of the GLA gene. These women may experience many of the classic features of the disorder, including nervous system abnormalities, kidney problems, chronic pain, and fatigue. They also have an increased risk of developing high blood pressure, heart disease, stroke, and kidney failure. The signs and symptoms of Fabry disease usually begin later in life and are milder in females than in their affected male relatives.

A small percentage of females who carry a mutation in one copy of the GLA gene never develop signs and symptoms of Fabry disease.