Swine Flu

Swine Flu!

Is it dangerous?

Swine influenza (also called pig influenza, swine flu, hog flu and pig flu) is an infection by any one of several types of swine influenza virus. Swine influenza virus (SIV) or S-OIV (swine-origin influenza virus) is any strain of the influenza family of viruses that is endemic in pigs.[2] As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H3N1, H3N2, and H2N3.

Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human influenza, often resulting only in the production of antibodies in the blood. If transmission does cause human influenza, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection. The meat of an infected animal poses no risk of infection when properly cooked.

During the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.

GOUT

Gout is a disease hallmarked by elevated levels of uric acid in the bloodstream. In this condition, crystals of monosodium urate (MSU) or uric acid are deposited on the articular cartilage of joints, tendons, and surrounding tissues. It is marked by transient painful attacks of acute arthritis initiated by crystallization of urates within and about the joints and can eventually lead to chronic gouty arthritis and the deposition of masses of urates in joints and other sites, sometimes creating tophi.

The crystals inside the joint cause intense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore if it is even slightly touched. For example, a blanket or even the lightest sheet draped over the affected area can cause extreme pain.

Gout usually attacks the big toe (approximately 75 percent of first attacks); however, it also can affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, or spine. In some cases, the condition may appear in the joints of small toes that have become immobile due to impact injury earlier in life; the resulting poor blood circulation can lead to gout.

Prevention strategies include reducing the supply of purine, dissolving crystals of uric acid so the uric acid can return to the blood, and increasing the excretion of uric acid from the blood into the urine, without causing lithiasis there. Prevention tactics involve careful diagnosis of the factors contributing to the gout, followed by appropriate use of medication, diet, and over the counter remedies.

Javanese poople (Indonesia) use some herbals to treat gout such as : Zingiber aromaticun (Lempuyang), Sida rombifolia (Sidaguri), Curcuma domestica (kunyit), Zingiber officinale var. Rubrum (jahe merah), Andrographis paniculata (Sambiloto), Imperata Cylindrica (alang-alang), Sonchus arvensis (tempuyung), Equisetum debile (Greges otot), Nigela sativa (Black cumin/habbatusauda)

URIC ACID

Uric acid is produced by xanthine oxidase from xanthine and hypoxanthine, which in turn are produced from purine. Uric acid is more toxic to tissues than either xanthine or hypoxanthine.

In humans and higher primates, uric acid is the final oxidation (breakdown) product of purine metabolism and is excreted in urine, over half the antioxidant capacity of blood plasma comes from uric acid. About 70% of daily uric acid disposal occurs via the kidneys, and in 5-25% of humans impaired renal (kidney) excretion leads to hyperuricemia.

Excess serum accumulation of uric acid can lead to a type of arthritis known as gout.

Elevated serum uric acid (hyperuricemia) can result from high intake of purine-rich foods, high fructose intake (regardless of fructose's low glycemic index (GI) value) and/or impaired excretion by the kidneys. Saturation levels of uric acid in blood may result in one form of kidney stones when the urate crystallizes in the kidney. These uric acid stones are radiolucent and so do not appear on an abdominal plain x-ray or CT scan. Their presence must be diagnosed by ultrasound for this reason. Very large stones may be detected on x-ray by their displacement of the surrounding kidney tissues. Some patients with gout eventually get uric kidney stones.

Gout can occur where serum uric acid levels are as low as 6 mg/dL (~357µmol/L), but an individual can have serum values as high as 9.6 mg/dL (~565µmol/L) and not have gout.

Sources of uric acid :
* In many instances, people have elevated uric acid levels for hereditary reasons. Diet may also be a factor; eating large amounts of sea salt can cause increased levels of uric acid. (Medical consultation is recommended before using large quantities of sea salt in daily cooking.)

* Purines are found in high amounts in animal internal organ food products, such as liver. A moderate amount of purine is also contained in beef, pork, poultry, fish and seafood, asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran and wheat germ.

* Examples of high purine sources include: sweetbreads, anchovies, sardines, liver, beef kidneys, brains, meat extracts (e.g. Oxo, Bovril), herring, mackerel, scallops, game meats, and gravy.

* Moderate intake of purine-containing food is not associated with an increased risk of gout.

* Serum uric acid can be elevated due to high fructose intake, reduced excretion by the kidneys, and or high intake of dietary purine.

* Added fructose can be found in processed foods and soda beverages as sucrose, or in some countries, as high fructose corn syrup.