The war between big time losers jÄgarna and we, the supreme awesomenesspeople, hb0da has been stepped up. In an interview with fascist bubblegum-newsmedia Onlinegamer.se, the obnoxious and aptly named Marjasin stated that hb0da were jÄgarna-wannabes. This could not be further from the truth and as a fact of the matter, it would more likely be the other way around. When hb0da-traitor and jÄgarna explosiveman Morf earlier this week attempted to disgrace the good name of hb0da in the same aforementioned media, he was soon put to shame by yours truly, and later also by the yapping Marjasin.

There will be blood.

My hovercraft is full of eels.

<TCM|weqo> Vilka spelare tror du kommer att ta sig in i landslaget?

<ulvbot> Jag skulle gissa på desamma som varit med förr, fast med vissa justeringar med tanke på de förändringar skett. Några tidigare kanditater faller ut, några nya talanger letar sig in. Men kärntruppen är säkerligen garanterad att innehålla Bybben, Glufse, Ryb, Appe och Weqo.

 <TCM|weqo> Låter troligt. Du nämnde dock ingen medic. Vem tror du kommer att få den rollen?

<ulvbot> Om inte Lezek kan lockas till comeback får förmodligen någon av de andra i laget byta klass och heala. I övrigt är hatE det hetaste alternativet.

<TCM|weqo> Tror du att Lezek är ett lämpligt alternativ och skulle han hålla måttet efter att inte ha spelat division 1 på flera månader, och dessutom vart helt inaktiv sen han slutade i jÄgarna?

<ulvbot> Med lite övning blir han helt säkert det bästa alternativet ändå. Hållpunkten blir väl snarare viljan. Min personlige favorit är dock Osten.

<TCM|weqo> Vilka nya svenska talanger skulle du se som alternativ för landslaget?

<ulvbot> Det enda tänkbara alternativet är wltrs som reservscout, då han är den enda i division 1 som inte är med i landslaget nu. Annars skulle det väl vara en eller ett par snubbar från jÄgarna som har en chans att ta plats, och kanske sQVEh från hb0da, men den chansen är ju minimal, med tanke på weqos hat mot lower divs.

<TCM|weqo> Vad tror du om sveriges chanser? Vilka länder kommer ge starkast motstånd?

<ulvbot> Det finns bara Finland och Sverige.

<TCM|weqo> Hur tror du det kommer att gå för våra norska grannar?

<ulvbot> Med skre långt borta och Treigzak förmodligen ur gammal god scoutform kommer västfolket få det mycket tufft. Det gäller att Braffle kommer tillbaks snart, annars kommer det bli en seg turnering för Torden och Dr.Leon. Eller snarare, en jättesnabb turnering.

<TCM|weqo> Då får jag be om att få tacka för intervjun och önska dig lycka till i ditt hejande på mig.

<ulvbot> Klart jag hejar på dig.

From Wikipedia, the free encyclopedia

The pathophysiology of hypertension is an area of active research, attempting to explain causes of hypertension, which is a chronic disease characterized by elevation of blood pressure to various degrees. Hypertension can be classified as either essential or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient’s condition. About 90-95% of hypertension is essential hypertension.^[1][2][3][4] While secondary hypertension indicates that the high blood pressure is a result of another underlying condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.^[5]

Most mechanisms leading to secondary hypertension are well understood, while pathophysiology of essential hypertension remains an area of active research, with many theories and different links to many risk factors.

A diagram explaining factors affecting arterial pressure

Cardiac output and peripheral resistance are the two determinants of arterial pressure. and so blood pressure is normally dependent on the balance between cardiac output and peripheral resistance.^[6] Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles.

Genetics

Evidence for genetic influence on blood pressure comes from various sources.^[7] Its proved that there is greater similarity in blood pressure within families than between families, which indicates a form of inheritance.^[8] And it was proved that wasnt due to shared environmental factors.^[9] Single gene mutations is proved to cause Mendelian forms of high and low blood pressure.^[10] almost 10 genes have been identified to cause this forms of hypertension.^[10][11]These mutations affect blood pressure by altering renal salt handling.^[12] Recently and with the aid of newly developed genetic analysis techniques researchers found statistically significant linkage of blood pressure to several chromosomal regions, including regions linked to familial combined hyperlipidemia.^{[13][14][15][16][17]} These findings suggest that there are many genetic loci, each with small effects on blood pressure in the general population. Overall, however, identifiable single-gene causes of hypertension are uncommon, consistent with a multifactorial cause of essential hypertension.^{[2][7][18][19]}

The best studied monogenic cause of hypertension is the Liddle syndrome, a rare but clinically important disorder in which constitutive activation of the epithelial sodium channel predisposes to severe, treatment-resistant hypertension.^[20] Epithelial sodium channel activation resulting in inappropriate sodium retention at the renal collecting duct level. Patients with the Liddle syndrome typically present with volume-dependent, low renin, and low aldosterone, and hypertension. Screenings of general hypertensive populations indicate that the Liddle syndrome is rare and does not contribute substantially to the development of hypertension in the general population.^[21]

Autonomic nervous system

Also the autonomic nervous system, plays a central role in maintaining the cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. Done by altering peripheral vasculature, and kidneys, causing increased cardiac output, increased vascular resistance, and fluid retention. Disorder of the system, as in case of sympathetic nervous system overactivity, increases blood pressure and contributes to the development and maintenance of hypertension.^[22][23] In addition, autonomic imbalance (ie. increased sympathetic tone accompanied by reduced parasympathetic tone) has been associated with many metabolic and hemodynamic abnormalities that result in increased cardiovascular morbidity and mortality.^[24][22]

The mechanisms of increased sympathetic nervous system activity in hypertension are complex and involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized.^[8][25][26] Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II.^[27][28] Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin.^[29][30] Some studies shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls.^[31] And that hypertensive patients doesn’t show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and its believed that this abnormal response is genetically inherited.^[32]

Exposure to stress increases sympathetic outflow, and repeated stress-induced vasoconstriction may result in vascular hypertrophy, leading to progressive increases in peripheral resistance and blood pressure.^[2] This could partly explain the greater incidence of hypertension in lower socioeconomic groups, since they must endure greater levels of stress associated with daily living. Persons with a family history of hypertension manifest augmented vasoconstrictor and sympathetic responses to laboratory stressors, such as cold pressor testing and mental stress, that may predispose them to hypertension. This is particularly true of young African Americans. Exaggerated stress responses may contribute to the increased incidence of hypertension in this group.^[33]

Renin-angiotensin-aldosterone system

Another system maintaining the extracellular fluid volume, peripheral resistance and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume, and arterial vasoconstriction, Thus it contributing to regulation of the blood pressure, it performs this function through breaking down (hydrolyzes) angiotensinogen secreted from the liver into the peptide angiotensin I, Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium, that enzyme is angiotensin converting enzyme (ACE) producing angiotensin II, the most vasoactive peptide.^[34][35]Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries and thereby raises the peripheral resistance, and so elevates blood pressure. Angiotensin II also acts on the adrenal glands too and releases Aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water leading to raised blood volume and raised blood pressure. So elevation of renin level in the blood, which is normally in adult human is 1.98-24.6 ng/L in the upright position.^[36] will lead to hypertension.^[37][2]

Recent studies claims that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue,^[38][39] and also linked renin-angiotensin system with insulin resistance, and claims that anyone can cause the other.^[40] Local production of angiotensin II in various tissues, including the blood vessels, heart, adrenals, and brain, is controlled by ACE and other enzymes, including the serine proteinase chymase. The activity of local renin–angiotensin systems and alternative pathways of angiotensin II formation may make an important contribution to remodeling of resistance vessels and the development of target organ damage (ie. left ventricular hypertrophy, congestive heart failure, atherosclerosis, stroke, end-stage renal disease, myocardial infarction, and arterial aneurysm) in hypertensive persons.^[37]

Endothelial dysfunction

The endothelium of blood vessels produces an extensive range of substances that influence blood flow and, in turn, is affected by changes in the blood and the pressure of blood flow. For example, local nitric oxide and endothelin, which are secreted by the endothelium, are the major regulators of vascular tone and blood pressure. In patients with essential hypertension, the balance between the vasodilators and the vasoconstrictors is upset, which leads to changes in the endothelium and sets up a “vicious cycle” that contributes to the maintenance of high blood pressure. In patients with hypertension, endothelial activation and damage also lead to changes in vascular tone, vascular reactivity, and coagulation and fibrinolytic pathways. Alterations in endothelial function are a reliable indicator of target organ damage and atherosclerotic disease, as well as prognosis.^[41]

Multiple evidences suggest that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension.^[42][43][44] Normally nitric oxide is an important regulator and mediator of numerous processes in the nervous, immune and cardiovascular systems, including smooth muscle relaxation thus resulting in vasodilation of the artery and increasing blood flow, suppressor of migration and proliferation of vascular smooth-muscle cells.^[2] It has been suggested that angiotensin II enhances formation of the oxidant superoxide at concentrations that affect blood pressure minimally.^[45]

Endothelin is a potent vasoactive peptide produced by endothelial cells that has both vasoconstrictor and vasodilator properties. Circulating endothelin levels are increased in some hypertensive patients,^[46][47][46] particularly African Americans and persons with hypertension.^{[48][46][49][50]}

References

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Maybe a Sneis-LAN is in order?

On wednesday san returns to the realm and on thursday we’ll play again. Oh wait, then its friday again. GOOD WEEK! LOL! :>

The day has come. It’s this day now. Today. There is no day quite like it. QQ

is todays horizon

Welcome Jowy! We’ve found our soldier, volleyball and whatever-else-they-might-like-to-do partner for Bananen.

Capocannoniere

Tremble fools and girlies, hb0da returns after a while in dormant state, to Team Fortress 2. We are still going strong and we are sure to beat just about everyone. Everyone! Yes, them too! The ones you thought about. It’s inevitable. The new line up isnt really new, its a bit old. Here it is.

• h.ulv - medic
• h.Bananen - soldier
• h.sneis - soldier
• h.san - demo
• h.sQVeh? - scout
• h.POOCAP - scout
• h.Blöjan - backup scout

Thats it. Enjoy us.

Bananen, the spy, and sQVeh, the sniper are farming for new weapons.

+attack

Sparven power.

Introducing for the first time on earth, the intergalactic supercosmic BANANEN FANCLUB with gazillions of members among the eSport fans throughout the galaxay. Now the fanclub expands to earth, and anyone willing to join this fanclub can sign up right away! There is no entry fee, and the initiation ritual is not that tricky. It does however involve a banana.

Bananen, of everlasting fame from glorious days on Lokalen and in in hb0da, currently playing for FakkelBrigade 2 has been a soldier without mercy for over a year now and I guess this is a tribute to him.

<3

<3

• here it is

In an effort of blood, tears and sweat, we now bring you…

THE LIST OF HOW DIVISION 1 IN ETF2L SEASON 5 WILL END! This list has no ties to any political institutions or any other such entity. We will also present a motivation which in every case can be credited to the four winds of the unstable mind.

1. Dignitas

• Four Kings forgot to win one of those previous seasons. This time they’ll remember.

2. Crack Clan

• They’ve got all the other good players.

3. FakkelBrigade

• Im doing this to please Dr. Leon. Yes, they’ll beat all those other awesome teams. And why? I leave that to the world to ponder upon.

4. Trademark Gamers

• They have… I dont know what they have. They’ve won before tho, and they can do it again. Lacking some stuff tho. They had it, now they dont. Fu!

5. Team CoolerMaster

• (folded)

6. Weapons of the Rebelion

• These guys are the best of what’s left too, and they have some experience playing top level on a regular basis here in Div 1, so that will… do it.

7. Weapons of the Rebelion 2

• They’ll be awesome.

8. Clan00

• They have Fragga.

9. Team YoYo Tech

• Yo! Yeah well, somebody has to lose.

10. The Imperial

• Nah, not really.

On a surprising note, I can’t say which team will be first to fold, but if had HAD to guess, I would say TCM, then Clan00. Then YoYo, then TmG.

Then Dignitas!