Discovery of Artificial Blood

In 1933, the American Clark and Gollan kept some mice immersed in a liquid which flooded their lungs and should have killed them. But they stayed alive. This fluid was an emulsion of a fluorocarbon in water. These fluorocarbon molecules link up with significant quantities of oxygen present in the water. This showed the beginnings of the invention of the blood substitute. In 1967, the American, Henry A. Sloviter injected the fluorocarbon emulsion into some rabbits along with the physiological liquid and some albumen. He also found that if the injected liquid is above a third in volume with respect to the blood, then the animal may die, because the substitute liquid cannot efficiently transport oxygen and carbon dioxide. The Japanese, Ryochi Naito carried out the first experiment on man by injecting himself with 200 ml of Fluosol DA, a milky looking artificial blood.

Syringe invention

The French doctor Velpeau made some observations on aneurysms. He pricked a needle into an aneurysm and noticed the formation of a clot. In 1835, the French doctor Charles Gabriel Parvaz invented the hypodermic syringe for injecting ferric chloride. The syringe was made up of a silver cylinder and the lid of the pump body could be screwed down; the cylinder had a nozzle to which the cannula could be fixed, which was itself extended by a steel trocar. Fournier invented the glass syringe in 1895. To eject the liquid, a piston which could be pushed down quite easily was used. In 1946, Blaise Pascal made a syringe for scientific use. With this syringe, purgative clysters were administered.

What happens once the DNA from the HIV particle enters the cell nucleus?

When physicians in Los Angeles and other cities noted an unusually large number of opportunistic microbial infections. Destruction of T lymphocytes of the immune system cells were associated with these infections, and it soon became obvious that an epidemic of disease was in progress. By 1984 the responsible virus had been identified, and in 1986 it was given the name human immunodeficiency virus (HIV). HIV is a very fragile virus, and for this reason it does not survive long periods of exposure outside the body.
In infected individuals, HIV infects T lymphocytes by combining its spike glycoproteins with the CD4 receptor sites of T lymphocytes. The nucleocapsid enters the cytoplasm of the T lymphocyte, and the viral enzyme reverse transcriptase synthesizes a DNA molecule using the RNA of HIV as a template (for this reason, the virus is called a retrovirus). The DNA molecule migrates to the cell nucleus and becomes part of a chromosome in the T lymphocyte nucleus.
The DNA molecule, known as a provirus, assumes a relationship with the DNA of the T lymphocyte, and the provirus enters the state of lysogeny. From this point in the nucleus, the provirus encodes new HIV particles, which acquire their envelope by budding through the membrane of the T lymphocyte. The human body attempts to keep up with the mass of new viral particles, but eventually the newly emerging strains of HIV overwhelm the body defenses and the T lymphocyte count begins to drop. Normally, it is approximately 800 T lymphocytes per cubic millimeter of blood, but as the disease progresses, the count drops into the low hundreds and tens. This drop may occur as soon as weeks after infection or as long as 20 years or more after infection. Thus far, vaccines are not available against HIV. Two glycoproteins called gp120 and gp160 from the envelope are being investigated as possible vaccines. Vaccine development is hampered however, since it is difficult to find volunteers who would become antibody- positive and could suffer discrimination as a result of antibody presence. Nevertheless, candidate vaccines have been prepared with gp120 and gp160. Many candidate vaccines are now in the testing stage