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Journal ArticleDOI
M.-T. King, D. Wild 
01 Oct 1983-Mutation Research
19 Citations
However, LPS-induced hypothermia as well as fever does not so far appear to produce cytogenetic damage.
Results show that a fever-like increase in temperature triggered apoptosis in dividing cell populations of testis and thymus, but not in mature, postmitotic cells of the adult cerebellum.
We suggest that leukocyte apoptosis associated with valvulopathy may be critical for the pathogenesis of Q fever endocarditis by deactivating immune cells and creating a favorable environment for bacterial persistence.
In the present study, evidence is provided demonstrating that bovine ephemeral fever virus induces apoptosis in several cell lines.
Supporting a role for P‐450 in endogenous antipyresis and antiinflammation includes evidence that (1) inducers of P‐450 reduce fever, (2) inhibitors of P‐450 cause a larger fever, (3) and P‐450 arachidonic acid metabolites reduce fever.
A natural rise of body temperature during mild fever can naturally accumulate high cellular levels of HSP70 that can arrest apoptosis and protect alveolar lung cells from inflammatory damages.
Open accessJournal ArticleDOI
C. Haanen, I. Vermes 
134 Citations
Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction.
Apoptosis, unlike coagulative necrosis, does not itself evoke an inflammatory response.
Here we show that fever-range hyperthermia accelerates the rate of neutrophil apoptosis at neutral pH but markedly increases neutrophil survival induced by low pH.
These findings link pyrin to apoptosis pathways and suggest that the modulation of cell survival may be a component of the pathophysiology of familial Mediterranean fever.

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What specific molecular pathways are activated in the ileum of mice after intraperitoneal LPS injection?
5 answers
After intraperitoneal LPS injection in mice, the ileum exhibits activation of specific molecular pathways. The injection of LPS leads to an increased inflammatory response, including elevated levels of IL-1β and IL-18 in serum, and the activation of the NLRP3 inflammasome in the intestine. Additionally, the expression of Slit2 and Robo4 decreases significantly in the intestine, while VEGF expression increases. Furthermore, there is a notable decrease in the protein levels of tight junction proteins like ZO-1, occludin, and claudin-5, which can be reversed by inhibiting the NLRP3 inflammasome. These findings suggest that the Slit2-Robo4 signaling pathway and tight junction proteins in the intestine play crucial roles in LPS-induced inflammation in mice, providing insights into the molecular mechanisms underlying sepsis.
What biological factors/mechanisms may underlie the development and maintanance of PTSD?
5 answers
The development and maintenance of PTSD may involve various biological factors and mechanisms. Neurobiological models suggest that PTSD symptoms can be influenced by neural mechanisms involving fear-related brain structures like the hippocampus, amygdala, and prefrontal cortex, which can undergo time-dependent changes. Epigenetic changes at the genomic and epigenomic level have been proposed to play a role in the susceptibility to PTSD after exposure to traumatic stress. Inflammation, particularly neuroinflammation, has been identified as a putative susceptibility factor for PTSD, with elevated levels of certain cytokines in the brain of susceptible individuals. Furthermore, biomarkers associated with neurodegenerative disorders, such as cerebral cortical thinning and immune-inflammatory alterations, have been linked to PTSD, potentially shedding light on the pathophysiological mechanisms connecting these conditions. Additionally, aberrant susceptibility of emotion- and fear-related neurocircuits, including the amygdala, prefrontal cortex, and hippocampus, may contribute to the development and retention of PTSD symptoms.
What are the cytokines involved with LAG-3 receptor from T helper cell?
4 answers
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4 answers
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5 answers
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5 answers
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4 answers
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