"උණ" හි සංශෝධන අතර වෙනස්කම්

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ටැග: ජංගම සංස්කරණය ජංගම යෙදුම් සංස්කරණය
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ටැග: ජංගම සංස්කරණය ජංගම යෙදුම් සංස්කරණය
11 පේළිය:
* මුඛය තුල උෂ්ණත්වය මැණීම - මෙහිදී උෂ්ණත්වය සෙල්සියස් අංශක 37.5 (ෆැරන්හයිට් අංශක 99.5) ට වඩා වැඩිනම් උණ ඇතැයි සැළෙකේ.
* කිහිල්ලේ උෂ්ණත්වය මැණීම - මෙහිදී උෂ්ණත්වය සෙල්සියස් අංශක 37.2 (ෆැරන්හයිට් අංශක 99) ට වඩා වැඩිනම් උණ ඇතැයි සැළෙකේ.
 
== ඇතිවන අයුරු ==
Temperature is regulated in the hypothalamus. Substances <!--"which" incorrect: NOT ALL substances induce fever; a distinction is to be made-->that induce fever are called ''pyrogens''. These are both ''external'' or ''exogenous'', such as the bacterial substance [[LPS]], and [[internal]] or [[endogenous]]. The endogenous pyrogens (such as [[interleukin 1]]) are a part of the [[innate immune system]], produced by [[phagocytic cells]], and cause the increase in the thermoregulatory set-point in the hypothalamus. The endogenous pyrogens may also come directly from tissue [[necrosis]].
 
[[ගොනුව:fever-conceptual.jpg|frame|right|'''Hyperthermia''': Characterized on the left. Normal body temperature (thermoregulatory set-point) is shown in green, while the hyperthermic temperature is shown in red. As can be seen, hyperthermia can be conceptualized as an increase above the thermoregulatory set-point.<br />'''Hypothermia''': Characterized in the center: Normal body temperature (thermoregulatory set-point) is shown in green, while the hypothermic temperature is shown in blue. As can be seen, hypothermia can be conceptualized as a decrease below the thermoregulatory set-point.<br />'''Fever''': Characterized on the right: Normal body temperature (thermoregulatory set-point) is shown in green. It reads “New Normal” because the thermoregulatory set-point has risen. This has caused what was the normal body temperature (in blue) to be considered hypothermic.]]
 
One model for the mechanism of fever is the detection of [[lipopolysaccharide]] (LPS), which is a cell wall component of [[Gram-negative|gram-negative bacteria]]. An immunological protein called [[Lipopolysaccharide-Binding Protein]] (LBP) binds to LPS. The LBP-LPS complex then binds to the [[CD14]] receptor of a nearby [[macrophage]]. This binding results in the synthesis and release of various [[cytokine]] factors, such as [[interleukin 1]] (IL-1), [[interleukin 6]] (IL-6), and the [[tumor necrosis factor-alpha]]. These cytokine factors are released into general circulation where they migrate to the circumventricular [[organ (anatomy)|organs]] of the [[brain]], where the [[blood-brain barrier]] is reduced. The cytokine factors bind with [[endothelium|endothelial receptors]] on vessel walls, or interact with local [[microglial cell]]s. When these cytokine factors bind, they activate the [[arachidonic acid]] pathway. This pathway (as it relates to fever), is mediated by the [[enzyme]]s [[phospholipase|phospholipase A2]] (PLA2), [[cyclooxygenase|cyclooxygenase-2]] (COX-2), and [[Prostaglandin|prostaglandin E2]] synthase (membrane-associated protein involved in eicosanoid and glutathione metabolism, also known as [[mPEGS-1]]). These enzymes ultimately mediate the synthesis and release of PGE2.
 
PGE2 is the ultimate mediator of the febrile response. The set-point temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts near the [[ventromedial preoptic]] area (VMPO) of the anterior [[hypothalamus]] and the [[parvocellular]] portion of the [[periventricular nucleus]] (PVH), where the thermal properties of fever emerge. It is presumed that the elevation in thermoregulatory set-point is mediated by the VMPO, whereas the neuroendocrine effects of fever are mediated by the PVH, [[pituitary gland]], and various [[endocrine organs]].
 
The brain ultimately orchestrates '''heat effector mechanisms'''. These may be
* increased heat production by increased [[muscle tone]], [[shivering]] and hormones like epinephrine and [[thyroid hormone]]s, or,
* prevention of heat loss, such as [[vasoconstriction]] or crawling under a blanket.
The [[autonomic nervous system]] may also activate [[brown adipose tissue]] to produce heat (=non-exercise associated thermogenesis, also known as non-shivering thermogenesis), but this seems mostly important for babies. Increased heart rate and vasoconstriction contribute to increased [[blood pressure]] in fever.
 
== වරගීකරණය ==
"https://si.wikipedia.org/wiki/උණ" වෙතින් සම්ප්‍රවේශනය කෙරිණි