OFFICIAL INSANITY THREAD

I always thought that those red blood cells were pretty tough to digest. Now I know why!

By the way, did you know that red blood cells are anucleate and filled with the oxygen carrying protein hemoglobin? No? Well, human erythrocytes are biconcave discs 7.5 microns in diameter. The biconcave shape provides a large surface-to-volume ratio for oxygen delivery and better flexibility in narrow capillaries. There are normally 3.9-5.5 million per microliter in women and 4.1-6 million per microliter in men. A decrease in the number of red blood cells is called anemia.

Within the cell membrane of erythrocytes is the respiratory pigment hemoglobin and enzymes to break down glucose. Erythrocytes loose their mitochondria, nucleus, ribosomes and many cytoplasmic enzymes during maturation to become specialized for carrying oxygen. Maturation in bone marrow takes 24-48 hours and the average red blood cell survives in circulation for 120 days. Old erythrocytes are removed from circulation by phagocytic cells of the spleen and bone marrow.

It's funny you mentioned Haemoglobin. I was just busy working out these facts about blood circulation:

Haemolysis of RBC involves the (i) rupture of the cell membrane and (ii) release of its cell content, haemoglobin. [86-4-(c)-(ii)]
Sodium oxalate solution is used to prevent blood clotting when taking samples. [86-4-(c)-(i)]
RBCs with lighter centre can be explained by having less cytoplasm and hence less haemoglobin. [91-1-(a)-(ii)-(1)]
The RBC which has a large surface area to volume ratio, is adapted to facilitate gaseous exchange. [91-1-(a)-(ii)-(2)]
RBC has a biconcave shape to provide a relatively large surface area to facilitate the diffusion of gases (NOT to carry more oxygen). [96-1-(b)-(iii)]
White blood cells can squeeze through the endothelial cell layer / lining of blood capillaries by amoeboid movement (NOT through diffusion). [89-2-(a)-(iv)]
Donor / recipient [87-1-(c)-(i)]
Persons with blood group AB cannot donate blood to all other blood groups; persons with blood group O cannot receive blood from other blood groups. [87-1-(c)-(i)]
In the classical Harvey's experiment, the purpose of tying the arm is to slow down blood glow to make the veins more conspicuous. [86-3-(c)-(iv)-(1)]
The thick and elastic wall of artery withstands / resists high blood pressure, but does NOT create or maintain it, NOR helps to pump the blood under high pressure. [92-1-(b)-(i)][96-1-(b)-(ii)]
The wall (NOT the cell wall) of the blood vessel is thick. [89-2-(a)-(i), (ii)][96-1-(b)-(ii)]
Distinguish between an artery and a vein with reference to the photomicrograph. [2000-3-(a)-(i)]
The increase in heart rate during vigorous exercise is to allow a faster blood supply to the muscle cells. (NOT to supply to all parts of the body, to the skin to promote heat loos, or to allow him to breathe faster in order to secure greater oxygen supply during exercise) [99-1-(b)-(i)]
If two subjects have similar demandn on blood and oxygen supply, the one with a lower heart rate has a heart which can pump out more blood in each beat. [99-1-(b)-(ii)]
The highly branched capillary netweork has a large surface area for efficient diffusion of materials, and a large total cross-sectional area which leads to a reduction in the rate of blood flow. [98-3-(a)-(i)]
The transport of substances : when oxygen, digested and absorbable nutrients are transported away from the site of absorption, it can maintain a steep concentration gradient across either the wall of the air sac [alveolus] or villus. [94-3-(a)-(ii)]
Comparison of the relative concentrations of carbon dioxide and glucose in the pulmonary artery and pulmonary vein. [92-1-(b)-(iii)]
Vena cava / renal vein [90-2-(c)-(i)]
Tissue fluid is formed by the hydrostatic pressure created at the arteriole end of the capillary bed which forces those substances small enough to pass through the capillary wall from blood (NOT by diffusion of substances from the blood across the wall of the capillary). [98-3-(a)-(ii)]
The continuous flow of lymph is maintained by the contraction of skeletal muscles (NOT nearby muscles) surrounding the lymph vessels (NOT by the pumping action of the heart), and the presence of valves in the lymph vessels (NOT in the veins, since the fluid is lymph but NOT blood) which can prevent the backflow of the lymph. [98-3-(a)-(iii)-(2)]

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REHAB IS FOR QUITTERS

Never knew you two were that iterested in blood, Hemoglobinopathies and Thalassemias anyone? Well let me tell you about it


I. Introduction
These conditions comprise a very large number of genetic biochemical/ physiological entities, most of which are academic curiosities whose major effect on medicine is to add to the surfeit of useless scientific information. However, several of these conditions (e.g., sickle cell anemia, hemoglobin SC disease, and some thalassemias) are common major life-threatening diseases, and some others (e.g., most thalassemias, hemoglobin E disease, and hemoglobin O disease) are conditions that produce clinically noticeable -- if not serious -- effects and can cause the unaware physician a lot of frustration and the hapless patient a lot of expense and inconvenience. We will study a few hemoglobinopathies and thalassemias of special importance. It should be kept in mind, though, that there are literally hundreds of diseases in these categories.

II. Definitions
Hemoglobinopathy: A genetic defect that results in abnormal structure of one of the globin chains of the hemoglobin molecule. Although the suffix "-pathy" would conjure an image of "disease," most of the hemoglobinopathies are not clinically apparent. Others produce asymptomatic abnormal hematologic laboratory findings. A very few produce serious disease. The genetic defect may be due to substitution of one amino acid for another (as with the very common Hb S and Hb C and the great majority of the other abnormal hemoglobins), deletion of a portion of the amino acid sequence (Hb Gun Hill), abnormal hybridization between two chains (Hb Lepore), or abnormal elongation of the globin chain (Hb Constant Spring). The abnormal chain that results may be the chain (Hb GPhiladelphia), chain (Hb S, Hb C), chain (Hb FTexas), or chain (Hb A2Flatbush). These abnormal hemoglobins can have a variety of physiologically significant effects, discussed below in greater depth, but the most severe hemoglobinopathies (Hb S and Hb C diseases) are characterized by hemolysis.

Thalassemia: A genetic defect that results in production of an abnormally low quantity of a given hemoglobin chain or chains. The defect may affect the , , , or chain, or may affect some combination of the , , and chain in the same patient (but never the and chain together). The result is an imbalance in production of globin chains and the production of an inadequate number of red cells. The cells which are produced are hypochromic/microcytic and contain a surfeit of the unaffected chains which cannot stoichiometrically "mate" with the inadequate supply of thalassemic chains. These "bachelor" chains can produce adverse effects on the red cell and lead to destruction of the red cell in the marrow (ineffective erythropoiesis) and in the circulation (hemolysis). Note that these two definitions are not mutually exclusive -- some hemoglobinopathies may also be thalassemias, in that a structurally abnormal hemoglobin (hemoglobinopathy) may also be underproduced (thalassemia). Some, but not all, hemoglobinopathies and thalassemias are hemolytic anemias. These nosologic concepts are summarized by the Venn diagram below.



III. Pathophysiology of hemoglobinopathies
Messing around with the amino acid sequence of a globin chain has something of a red kryptonite effect. While some positions on the protein chain can tolerate a lot of substitutions without compromising the physiologic integrity of hemoglobin, other positions are very sensitive to amino acid substitutions. For instance, substitution of valine or lysine for glutamate at position 6 of the chain produces hemoglobins S and C, respectively, which form intraerythrocytic tactoids (see below) and crystals (again respectively) that cause premature destruction of the rbc (hemolysis). On the other hand, substitution of glutamate, asparagine, and threonine for lysine at position 59 of the chain produces, respectively, hemoglobins IHigh Wycombe, JLome, and JKaoshiung, all of which are physiologically indistinguishable from normal Hb A. Without venturing too deeply into tedious stereochemistry, we can say that abnormal globin structure can functionally manifest itself in one or more of the following ways:

Increased O2 affinity
These hemoglobins tend to result when mutations affect the portions of the amino acid sequence that compose 1) the regions of contact between and chains, 2) the C-terminal regions, and 3) the regions that form the pocket which binds 2,3-DPG. The hemoglobin eagerly scarfs up the O2 from the alveoli but then only stingily gives it up to the peripheral tissues. The kidney, always compulsively vigilant for hypoxia, cranks out the erythropoietin thinking that a few extra red cells might help out matters. Erythropoiesis then is stimulated, even though there is no anemia, and erythrocytosis (increased total body rbc mass, increased blood hemoglobin concentration, increased hematocrit) is the result.

It is important to know that these rare increased O2 affinity hemoglobins exist to prevent diagnostic errors from occurring in working up patients presenting with erythrocytosis (which is much more commonly caused by other conditions, including polycythemia vera [a neoplasm], cigarette smoking, psychosocial stress, chronic residence at high altitudes, and chronic lung disease). Examples of these include Hb Chesapeake and Hb JCapetown.


Decreased O2 affinity
This is the other side of the coin. These hemoglobins are reluctant to pick up O2 from the lung. The result is a decreased proportion of hemoglobin that is oxygenated at a given PO2. The remainder of the hemoglobin is, of course, deoxygenated and is blue. If the level of blue hemoglobin exceeds 5 g/dL in capillary blood, the clinical result is cyanosis, a bluish discoloration of skin and mucous membranes.

Again, it is important to know about these hemoglobins and keep them in the back of your mind when working up cases of cyanosis, a condition much more commonly caused by pulmonary dysfunction or right-to-left cardiovascular shunts. Examples of low O2 affinity hemoglobins include Hb Seattle, Hb Vancouver, and Hb Mobile.


Methemoglobinemia
These hemoglobins are a special class of low O2 affinity hemoglobin variants that are characterized by the presence of heme that contains iron in the ferric (Fe+++) oxidation state, rather than the normal ferrous (Fe++) state. These methemoglobins are all designated "Hb M" and further divided by the geographic site of their discovery, e.g., Hb MSaskatoon and Hb MKankakee. The affected patients have cyanosis, since the methemoglobin is useless in O2 binding.

Methemoglobinemia due to hemoglobinopathy should be distinguished from methemoglobinemia due to other causes, such as NADH-diaphorase deficiency. This enzyme is needed for the reduction (to heme) of metheme that accumulates as a result of normal metabolic processes. Congenital absence of NADH-diaphorase causes an accumulation of metheme, despite the fact that the structure of the globin chain is normal. Toxic methemoglobinemia occurs in normal individuals exposed to certain oxidizing drugs and other compounds in the environment, even though these individuals have normal hemoglobin structure and a normal complement of NADH-diaphorase. In such victims, the oxidizing power of the toxin overwhelms the normal antioxidant defenses.

Since methemoglobin is a brown pigment, patients with clinically severe methemoglobinemia have obviously brown blood. This observation allows one to make a clever and memorable diagnosis at the bedside during the patient's first venipuncture.


Unstable hemoglobin (Heinz body anemia)
Certain abnormalities in the globin chain sequence produce a hemoglobin that is intrinsically unstable. When the hemoglobin destabilizes, it forms up into erythrocyte inclusions called Heinz bodies. It is important to know that Heinz bodies are not visible in cells stained with the routine Wright stain. It is necessary for the cells to be stained with a supravital dye (such as brilliant cresyl blue, which can also be used to demonstrate reticulocytes) to be visible. These inclusions attach to the internal aspect of the rbc membrane and reduce the deformability of the cell and basically turn it into spleenfodder. The result is hemolytic anemia. All of these hemoglobins are rare; inheritance is autosomal dominant. Homozygotes have not been described. Examples of unstable hemoglobins are Hb Gun Hill, Hb Leiden, and Hb Köln.


Sickling and crystallization
These phenomena occur respectively in Hb S and Hb C, the most important of the abnormal hemoglobins. We will deal with these in greater depth next.

IV. Specific hemoglobinopathies
A. Hemoglobin S and sickle cell disease
1. Epidemiology and genetics
The Hb S gene is found primarily in populations of native tropical African origin (which include most African-Americans). The incidence of the gene in some African populations is as high as 40%; in African-Americans the incidence is 8%. The gene is also found with less frequency in non-Indo-European aboriginal peoples of India and in the Middle East. Rare cases have been reported in Caucasians of Mediterranean descent. The gene established itself in the tropical African population presumably because its expression in heterozygotes (sickle cell trait) affords some protection against the clinical consequences of Plasmodium falciparum infestation. Unfortunately, homozygous expression produces sickle cell disease, which is a chronic hemolytic anemia and vaso-occlusive condition that usually takes the life of the patient.

Hemoglobin S has the peculiar characteristic of expressing its biochemical instability by precipitating out of solution and forming up into long microtubular arrays called tactoids. The erythrocytes which contain the Hb S stretch around the tactoids to form the characteristic long, pointed, slightly curved cells called (with somewhat liberal imagination) "sickle cells." Only the deoxygenated form of Hb S (deoxy-Hb S) makes tactoids. The greater the proportion of Hb S in the cell, the greater is the propensity to sickle. Therefore, persons with 100% Hb S (being homozygotes) sickle under everyday conditions, while typical heterozygotes (who usually have about 30-40% Hb S) do not sickle except possibly under extraordinary physiologic conditions. Since Hb S is a chain mutation, the disease does not manifest itself until six months of age; prior to that time the Hb S is sufficiently "watered down" by Hb F (22), which of course has no chain.

In post-infancy individuals homozygous for the Hb S gene, 97+% of the hemoglobin is Hb S, the remainder being the normal minor hemoglobin, Hb A2 (22). Several coexisting genetic "abnormalities" (actually godsends) prevalent in African populaitons may ameliorate the course of the disease:

-thalassemia carriers (which comprise 20% of African-Americans!) have a lower MCHC than normal individuals. It has been suggested that a low MCHC is beneficial in decreasing the vaso-occlusive properties of sickled cells. These sickle cell patients live longer and have a milder disease than do non-thalassemic patients. Thalassemia is discussed in greater detail below.


Hereditary persistence of fetal hemoglobin (HPFH) has established itself in the black population and allows Hb F to so dilute the Hb S that sickling does not occur or is less prominent. In these people the Hb F gene does not "turn off" in infancy but persists indefinitely.

G-6-PD deficiency has been suggested as an ameliorative condition for sickle cell disease. This is controversial; the pathophysiologic basis of any such effect must be pretty obscure.
2. Clinical findings
Sickle cell anemia is a particularly bad disease in that not only is it a hemolytic anemia, but also a vaso-occlusive condition. The clinical findings can then be divided into one of these two groups:
a. Effects of chronic hemolysis
Anemia. Pretty much self-explanatory
Jaundice, due to rapid heme turnover and subsequent generation of bilirubin
Cholelithiasis. It has been classically taught that sickle cell patients are prone to the formation of calcium bilirubinate gallstones due to excess bilirubin secretion into the hepatobiliary tree.
Aplastic crisis. Many of us have brief episodes of marrow aplasia as a result of common viral infections. With a normal erythrocyte life span of 120 days, no anemia results from an unnoticed marrow shut-down of a few days. However, the sickle cell patients, with their markedly abbreviated rbc life span, can have a precipitous fall in hematocrit (and retic count) under such conditions. This may be life-threatening.
Hemolytic crisis. Most sickle cell patients establish a stable, tonic level of hemolysis. Rarely, for obscure reasons, they experience a catastrophic fall in hematocrit, increasing intensity of jaundice, and increasing reticulocyte count. This is called a "hemolytic crisis."
b. Effects of vaso-occlusion
Dactylitis. Resulting presumably from infarction or ischemia of the bones of the hands and feet, this is often the presenting manifestation of sickle cell disease in a six-months-old infant. The hands and feet are swollen and painful.
Autosplenectomy. In childhood, the spleen is enlarged due to excess activity in destruction of the sickled erythrocytes. Gradually, the spleen infarcts itself down to a fibrous nubbin.
Priapism. This refers to a painful and sustained penile erection, apparently due to sludging of sickled cells in the corpora cavernosa. Sometimes the penis has to be surgically decompressed. Repeated episodes of priapism cause the spongy erectile tissues to be replaced by fibrous tissue, with impotence being the end result.
Renal papillary necrosis. The physiologic function of the loops of Henle make the renal medulla an eldritch, unbodylike area of high hematocrit, high osmolarity, low pH, hemodynamic stasis, and low PO2. All of these conditions predispose to sickling and infarctive loss of the papillae of the pyramids. The result is inability to concentrate and dilute urine. Even sickle cell trait individuals may experience episodes of hematuria, presumably due to this mechanism.
Infarctive (painful) crisis. Increased sickling activity may be brought about by any general stress on the body, especially infection. Almost any organ may suffer acute infarction (includinmg the heart), and pain is the chief symptom.
Sequestration crisis. This occurs mostly in infants and young children and is characterized by sudden pooling of sickled erythrocytes in the RES and vascular compartment. This produces a sudden fall in hematocrit. Sequestration crisis may be the most common cause of death in sickle cell patients in the youngest age group.
Leg ulcers. After all of the disasters mentioned above, this seems trivial. However, the deep, nonhealing ulcers of skin and tela subcutanea (classically around the medial malleolus) may be the only clinical manifestation of sickle cell disease in an otherwise well-compensated patient. These may be the only bugaboo standing between the patient and a productive, financially solvent life.

holy s h i t ! huh.... my hands would fell off if i'd try to type something like that.

I know something is copy/paste but still...

We should be fair to the others, Chris. If we talk about "Thalassemia" we should try to expalin it in plain english so that everyone knows what the experts like us refer to.

BETA THALASSEMIA MINOR (HETEROZYGOUS) (B+)
This is the most common of the thalassemias. Beta chain
production is less than normal due to the failure of one of the
genes coding for beta chains. Alpha chain production continues at a
near normal rate. The alpha chains combine with the available beta
chains resulting in decreased levels of hemoglobin A. There still
remains excess alpha chains and this stimulates the increased
production of delta chains. The alpha and delta chains combine to
form increased amounts of hemoglobin A2. If there is still an
excess of alpha chains the normal mechanism which switches off
gamma chain production does not function correctly and the rate of
gamma chain production is greater than in a normal adult. This
results in the formation of increased amounts of hemoglobin F.
Laboratory diagnosis of beta thalassemia minor
These patients are not severely anemic. The importance of
identifying heterzygous beta thalassemia is to prevent the
investigation and expense caused by confusion with iron deficiency.
As well these patients can then be provided appropriate genetic
counselling.
Hemoglobin, Hematocrit are decreased. The RBC count is not as
low as the hemoglobin and hematocrit, in fact it is usually normal.
This is due to the fact that the marrow can still produce the
cells but cannot fill them with hemoglobin. Hence the Hgb is low
and the empty cells occupy less space thus lowering the Hct
relative to the erythrocyte count.
Hemoglobin is very seldom, if ever, below 95 g/L. If the Hgb is
less than 93 g/L it is unlikely the patient has beta thalassemia
minor.
Morphology is microcytic and hypochromic. Anisocytosis is only
slight and not near as marked as in iron deficiency. This is
reflected in a near normal RDW and red cell histogram which is
shifted to the left but of near normal dimensions. There is slight
poik with an occasional target cell. A moderate basophilic
stippling is common.
Indecies show a characteristic discordance. The MCV is slightly
decreased and the MCH is decreased. The MCHC is normal. The RBC
number is usually normal.
The discriminant factor (DF) is a mathematic manipulation of
the indecies and generates a number which can be used to help
differentiate between thalassemia minor and iron deficiency. At
least three formulas are in use:
Mentzer: MCV
--- = if <13 then thal minor
RBC >13 then iron deficiency

Shine-Lal: (MCV)squared X MCH = if <1530 then thal minor
>1530 then iron deficiency

England-Frazer : MCV-(Hgb X 5)-RBC- 3.4 = if negative thal minor
positive iron def

The England-Frazer formula is the most often used.
White cell count and differential - normal

Retics - relative increase
PI decreased

Bone marrow - normal to slight erythroid hyperplasia.

Serum iron - normal
TIBC - normal
Ferritin - normal
Bilirubin - slight increase due to intramedullary hemolysis
FEP - normal

Hemoglobin studies:
Hgb A - decreased
Hgb A2 - increased
Hgb F - Sl increase to normal

BETA THALASSEMIA MAJOR (HOMOZYGOUS) (B0)
These patients are well at birth but develop a life threatening
anemia by one or two months. They must be supported with blood
transfusions which result in iron overload. Unless the iron is
removed with appropriate chelation therapy these patients die of
hemosiderosis.
In beta thalassemia major there is a complete failure of beta
chain production. Hence there is very little, if any, Hgb A present. Delta and gamma chain production is increased. As a result there is
raised levels of Hgb A2 and Hgb F. Hemoglobin F has a very high
affinity for oxygen and is a poor oxygen deliverer. As a result the
only functional hemoglobin present is Hgb A2, hence the patient is
hypoxic which causes increased erythropoietin secretion. The excess
erythropoietin stimulates the marrow to the maximum, and ultimately
to the point that extramedullary hemopoiesis occurs with
splenomegaly. Even with in increased production of hemoglobins A2
and F there are still excess alpha chains and they precipitate in
the developing normoblasts. This results in intramedullary
hemolysis and their premature removal from the marrow by RE
cells.
Laboratory diagnosis of beta thalassemia major
Anemia is severe - Hgb 20 to 30 g/L. Hematocrit and RBC count
are also decreased hence the indecies are uniformly depressed.
The MCV, MCH and MCHC are all decreased.
The RDW is increased.
The RBC histogram is shifted to the right and abnormal in shape due
to the presence of NRBC and abnormal RBC shapes.
The morphology is severe hypochromic microcytic with marked
aniso and poik. Many target cells, schistocytes, leptocytes (large
thin flat cells). The presence of these cells often makes it
difficult to recognize the microcytosis. Moderate basophilic
stippling and many NRBC are common.
The WBC is invariably increased when first performed but is
normal after correction for NRBC. The differential is usually
normal.
Retic count - relative increase 5 to 10% but the PI is
decreased.

Bone marrow - erythroid hyperplasia with dyserythropoiesis.
Stainable iron is increased and a rare ringed sideroblast may be
seen.
FEP normal to increased

Serum iron - increased/normal
TIBC - decreased/normal
Ferritin - increased/normal
%saturation - increased
Hemoglobin electrophoresis -
Hgb A - decreased
Hgb F - increased
Hgb A2 - variable

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REHAB IS FOR QUITTERS

Oh man. I didn't know everyone on this forum was so intelligent! I feel inadequate!

oooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooo
you all are nothing alse as crazy!!!



=============================================
=!!!!Michael S. and his team Ferrari rulz!!!=
=============================================

Don't be upset Zcott. You certainly know the chinese proverb
"A gem is not polished without friction, not a person perfected without trials."

Or as we say in Kioto, Japan (where I come from): "Nana korobi, ya oki"

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REHAB IS FOR QUITTERS

What's Jabber? huh.... its in the "edit profile" maybe some messenger?

Jabba the Hutt, the notorious crime lord who ran his organization from the planet Tatooine, was one of the major kingpins in the Outer Rim Territories. His organization was into a wide variety of illegal activities. From smuggling to spice dealing, slave trading to murder, loan sharking to protection, Jabba the Hutt had his bloated fingers in all the underworld's pies. Like others of his race, Jabba was a legless, sluglike being with reptilian eyes and gross mannerisms. Approximately four meters long, Jabba was huge even among his own kind. His desert palace on Tatooine was full of all kinds of decadent luxuries, an army of alien and human criminals, droid slaves, and fawning servents. Among Jabba's most prized possessions were the rancor and the sail barge. Every smuggler, bounty hunter, pirate, and thief in the Outer Rim Teritories eventyally took on a job for Jabba, including Han Solo and his partner Chewbacca.

In fact, it was because of a job Solo botched that Jabba ultimately met his end. After Solo dumped a shipment of spice to avoid an Imperial blockade, Jabba gave the smuggler a limited time to make good on the shipment's worth. When Solo failed to return to Tatooine to pay off his debt--he was off helping the Rebellion--Jabba put a price on his head. Boba Fett eventually collected the bounty, but Solo's Rebel companions came to rescue him. Among this group was Luke Skywalker. Although Skywalker's Jedi "mind tricks" did not work against Jabba, his other abilities made short work of the crime lord's men. It was Princess Leia, however, who actually killed Jabba. Since that time, other criminal organizations have been attempting to fill the void left by Jabba the Hutt's sudden and unexpected demise.

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REHAB IS FOR QUITTERS

Nice explanation, Vader.
hehe...
OK now i want the real answer :p

What is Jabber?
The coolest IM system on the planet

The first application of Jabber technology is an instant messaging system focused on privacy, security, ease of use, access from anywhere using any device, and interoperability with IM, phone, and web-based services. The result? Jabber is quickly becoming a standard component of Internet infrastructure.

A fun and productive open-source community

The heart of Jabber is a vibrant community of developers working at the intersection of XML, presence, and real-time messaging. Led by the Jabber Foundation, this community is building an open technology framework that enables freedom of communication among people, applications, and systems across all platforms. Visit the DevZone for further information and to download Jabber software.

A powerful platform for XML messaging and presence

Jabber is fully based on XML, so it provides an extensible architecture for creating the next generation of services and applications on the Internet. The benefits of using Jabber include presence management, transparent interoperability, and real-time routing of structured information.

A thriving commercial marketplace

Jabber gives businesses a standard, interoperable messaging platform that is flexible, scalable, and highly secure. As a result, a number of high-profile companies are now building and offering commercial services based on Jabber, led by the efforts of Jabber, Inc.


Go check

[jabber.org]

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REHAB IS FOR QUITTERS

Isn't this cute?

[www.jesus-is-lord.com]

The Duckbill Platypus


God made all the animals including the duckbill platypus. The platypus is a small furry little animal that loves the water (it's aquatic).

The platypus lives near fresh water where it finds its food and makes its home.



The platypus is a very unusual mammal (mammal means that it has fur on it):

It lays eggs like a bird or a reptile (this makes it a monotreme mammal)
The males have poison like a snake in spurs on their hind legs. The poison can kill a dog and cause extreme pain in people.
They have a bill like a duck.
They have a tail like a beaver.
They have webbed feet like a duck.
The mother's milk comes out through glands on her skin and the babies lick it off of her fur.
The platypus is only found in Australia and its island state, Tasmania.



The platypus lives a solitary life in and around fresh water spending about 12 hours a day swimming and searching for food in the water. They have voracious appetites and can eat their own body weight in food in one night! The platypus can remain submerged up to 2 or 3 minutes at a time. Since its nostrils are on top of its bill, it can breath as it swims on top of the water. If you want to see a good picture of a platypus swimming, click here.

The platypus likes to eat worms, slugs, shrimp, larvae, eggs and yappies. It lives in burrows that it digs under the ground near water. The burrow can be up to 20 yards (60 feet) long!



The mother platypus lays two eggs and keeps them warm by placing them on her belly and covering them with her tail. In about two weeks they are born. The baby platypi are naked and helpless. They drink their milk off of their mother's fur for four to five months. When she goes to get food they stay in the comfort of the burrow.

The platypus can live up to 17 years in captivity. It has dark brown fur on its back and silvery to light brown hair on its belly. It can grow up to two feet long including its tail. It is a shy little animal that keeps to itself. God takes care of the platypus.

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REHAB IS FOR QUITTERS

Yo Sup

I may as well join in

A forfeited game in baseball is recorded as a 9-0 score. In football it is recorded as a 1-0 score.
Anise is the scent on the artificial rabbit that is used in greyhound races.
Australian Rules football was originally designed to give cricketers something to play during the off season.
Bill Russell was the first black head coach of a major league pro sports team.
Canada is the only country not to win a gold medal in the summer Olympic games while hosting the event.
In the United States, more Frisbee discs are sold each year than baseballs, basketballs, and footballs combined.
Kite flying is a professional sport in Thailand.
Pole vault poles used to be stiff. Now they bend which allows the vaulter to go much higher.
The hammerthrow is illegal as a high school sport in all states except Rhode Island.
A hedgehog's heart beats 300 times a minute on average.

that;ll do for the moment




Racing Is Life. Anything that happens before or after is just waiting
Jesus may be able to heal the sick and bring the dead back to life, but he can't do shît for low fps

Donde estan las muertes, señor?

Did you know even Africa has a SEARCHBUTTON-MAN or close relative? There is a proverb in Swahili that goes like this: "Asking questions is not silly."


Here is a fine collection of assorted proverbs:

Where the cattle does not graze, the warriors pass."
- (Nilotic proverb)

"I have to learn how to walk on three legs says the hyena for when I am old".
- (Bambara proverb)

"If you shake a dog, you shake his owner".
- (Rwandan proverb)

(BTW: "Shake the dog" sounds rather naughty. But as our french friends would say: "Honi soit qui mal y pense"

An toir thu dhomh pòg? - Will you give me a kiss
Cha toir, ach bheir mi dhut sgailc! - No, but I'll slap you.
(scottish gaelic)

And to Ellis2kX how mentioned this topic on the other forum (the one about sheep and shepard, bypassing trains and footie-fans) here is this scottish-gaelic sentence (with pronounciation help):

"Cò an caora sin còmhla riut a chunnaic mi an-raoir?"
(Kaw uhn KEU-ra shin KAW-la root uh CHOO-nik mee uhn-royer?)
"Who was that sheep I saw you with last night?"

Or as the man from Kyoto said: "Kono ika o kette mo kamaimasen ka? (Do you mind if I kick this squid?)

Será possível que alguém me traga as malas para cima?


till than and don't forget:

abyssus abyssum invocat

Slán go fóill.

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REHAB IS FOR QUITTERS

This is crazy.

Ehmmm....

slovene:

Good morning!
Dobro jutro!

How are you?
Kako si?

good...
dobro...

You played GP3 today?
Si danes igral GP3?

Of course!!!
Seveda!!!



hehe
it is insanity thread, so there's nothing wrong with my post you actually learn new stuff :p

The second symphony and particularly the first movement is best characterized as being merry and tender. Many listeners have heard it and suggested it was a "glimpse of nature, a spring day amid soft mosses, springing woods, birds notes, and the bloom of flowers." (Specht, Richard). There is a very strong sense of metaphor with the work, although much like Beethoven, the metaphorical components do not interfere with the structure of the work~~we get the feeling that this means something more for our interpretation but it is not stated specifically. It is noted that Brahms was inspired by the lovely country and surrounding of southern Austria. Therefore, it would seem as though the sense of metaphor could directly relate to what Brahms was feeling at the countryside: peaceful, serene, joyful, playful, etc. In another sense, we can think of the movement as a whole solely based on simplicity, thus denoted with the opening motive in the first measure. In essence, we can see the complexity of ideas throughout the piece strain from simple thoughts, which again, could be the general feelings of Brahms at the time. In retrospect feeling the gentleness and calmness of the countryside compared to that of the city areas. We can see those ideas very clearly in this piece.

In the comparison of Brahms and Beethoven, I think it would be most helpful to point out Beethoven's tendencies and innovations since he had a direct influence on Brahms. Essentially, Beethoven's innovations occurred through three main stages of his life. The first period he starts to use the different impacts of piano and forte and unexpected outbursts with leaping arpeggiated figures known as "Mannaheim rockets." He expands the form (long and polythematic expositions). Throughout the middle period, or the heroic period, he is much more improvisatory and innovates the sonata structurally by creating shorter expositions and making the development and coda longer. The third period is basically focused on romantic tools, lyricism and increased counterpoint.

Beyond these points, Beethoven has some addition personal tendencies:
1. usually stick with diatonic/triadic complicity. Most themes are derived from a tonic triad (very classical)
2. he juxtaposes unrelated tonal areas without any preparation
3. demonstrates that key relationships are important in the harmonic colour of his music, no the keys themselves (long range handling of harmony)
4. creates surprise (rockets, piano, forte, etc.)
5. rhythmic vitality created by motifs, use of harmonies, syncopes, offbeat accents, and a mastery of dynamics.
6. inversion of chords
7. contrary motion of 3rds
8. more music in the recap than in the exposition
9. harmony puzzle or instability at the outset of piece (tension and suspense)

Beethoven's influences on Brahms includes the relentless rhythmic drive, beautiful breadth of melodies, originality of modulations, dramatic treatment of the main structural landmarks, and particular expressive content. Furthermore, Brahms at times has the same key relationships as Beethoven which is why he is often critisized for follow Beethoven's harmonic structure too much. Another similarity and transcending aspect from Beethoven, is Brahms' use of contour by using descending 3rds.

Generally speaking, Brahms sticks to the late sonata form which Beethoven helped to develop. His writing is more classic in some regards than Beethoven in terms of harmonic structures used, parallel third movement, and simple, short themes. Also, Brahms is not a user of the unexpected outbursts as much as Beethoven is. On the other hand, there are times when Brahms is very romantic in regards to his lyricism and expression. Much like Beethoven did, when he exhausted the tools of the classical style, he turned to new ways of expression and new kinds of content. Metaphorically speaking, Beethoven ushered in the use of metaphor and although it seems like it took Brahms' a little longer to settle into it, his since of metaphor is great just as well.
One interesting note on the comparison of the first two key areas is that it does not follow the traditional sonata-allegro tonal plan, that is going from the major tonic to the dominant. At the second key area (mm 82), the arpeggio and cello melody outline f# minor, or the iii, which makes this tonal relationship somewhat different compared to that of the classical style. The tonal areas are similar in thematic textures and sense of metaphor. Also, the transitions contain thematic fragments of the initial motive. You can see influence of the "x" motive at 82, thus being the same step wise motion in the cellos, only variation in harmonic rhythm. The rhythmic context of the motive may be implied by the two pizzicato notes, however that is not entirely evident.

Thematic fragments from the first key area are denoted in the score. In terms of size of each section, the development section is slightly shorter than the exposition, which may be a little different than what Beethoven did structurally at times.

The size of the coda still qualifies it as a separate section. After debating on this for several days, I initially thought that the coda was a simple extension of the winding down of the recapitulation and intertwines the original motive. However, I do think the coda is a separate section, if only for the reason that it is such a dramatic texture change. It does bring us back to the motives of the first key area, and closes with variations on that motive at 497. In this case, I think size is irrelevant. In essence, if I continue with my point before, that this is based on the simplicity of the motive, this particular section (coad) is what brings us home to that idea from the recapitulation, so yes, it is a separate section. Coincidentally, I think this coincides with the character change at the end and the fact that Brahms does not end in a powerful fashion. In the metaphorical sense, I think Brahms is seeing the countryside again here, just as he was at the beginning~~he wants to leave us with that relaxed, somber feeling. In a sense, he is bringing us back home and putting us back to sleep where he awoke us from; we have cycled ourselves back to the beginning of the work.

One other point of interest, is the debate on rather or not the first statement to the timpani role is the actual first tonal area or is merely the introduction to the rest of the piece. After debating this for a couple of weeks, I'm still not sure what Brahms had in mind for the opening. I have decided that it is the first tonal area, however I can make a case for it being an introduction. However, as I am typing, it has occurred to me that Brahms knew what he was doing when he put the repeat in the second bar which I have not paid attention to. I think maybe the first measure is the introduction, but serves more as an inhale of a motive to be exhaled out through the rest of the piece?

Here's a good fact: The Altavista language translator is a complete joke! I always enjoy having a bit of fun with it... writing out a passage in English, translating it to Korean or some other obscure language (no offence intended), then translating it back to English. If you haven't yet appreciated the comic value of this process, let me give you an example. I will translate this passage from ENGLISH ---> KOREAN -----> ENGLISH. Let's Go...
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From here is a good fact,: The Altavista language interpretation is
the joke which is complete,! I always inside Great Britain fun in
small quantity to it... It writes from transit, it has, it enjoys and
when it, it translate it it faces each other the that time English
back, a Korean or el that outside of E for dark language in (violation
which is prearranged) it translate. When you do not evaluate the
comedy value of this process still, it sees to me it gives in you,
make. I will translate transit from British ---> Korean ----->
English. Go...
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And there you have it! What fun! It makes no sense whatsoever!




HISTORIC BTCC VIDEOS

roflmao that is great!!!!!!!!!!!!

At our old primary school there was a computer which one day spoke whatever you typed! Seeing as we were little kids we thought it woul be funny to write swear words in it, the computer completely froze and teachers couldnt turn it of and it just keept repeating "@#$%&, c.r.a.p , s.h.i.t" really loudly. That day was sooooooo funy, no-one could concentrate in lessons and no-one would admit to it


heheheheheheheehehehehehe

British ---> Korean -----> English
LOL

yeah there's no translator on the net that would do its job FINE.