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The results show that FIP decreases dramatically with an increase in the mudcake permeability.
It should be noted that FIP and fluid loss pressure (FLP the critical wellbore pressure causing mud loss into the fracture) should be distinguished from each other.
It can be observed that FIP has a significant enhancement with an increase in the mudcake thickness, implying that the wellbore can be better strengthened by a thicker mudcake.
However, the result is consistent with other studies demonstrating higher incidence of FIP in cats below 2 years of age [ 5, 11, 14] and agree with the fact that FIP is a disease of young cats.
A long-standing hypothesis is that FIP viruses arise from internal mutation of endemic FECVs (12 ), which is believed to occur in approximately 1%–5% of enteric infections, resulting in the ability of the virus to infect blood monocytes and tissue macrophages.
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Liu et al. found that FIP-fve could be applied in local nasal immune therapy to suppress allergic responses to house dust mite allergy in Balb/c mice [ 70], and a shift in cytokine profile towards a stronger Th1-response was also noted in this study.
Our own observations ([ 72], and unpublished results) indicate that natural FIPs or cloned FIPs from Flammulina or Ganoderma have a limited effect on NO production in RAW 264.7 cells (a murine monocyte cell line), and a Th1-skewing effect in human PBMC cultures from healthy volunteers.
The fact that the FIP worker is separate from social workers means parents are less suspicious of them – and they can be more hands on.
These findings demonstrate that in FIP cases FCoV type I predominates, too, nonetheless, in 14% of the cases FCoV type II was detected, suggesting its causative involvement in cases of FIP.
The above analysis has shown that increased FIP and thus wellbore strengthening can be achieved by forming a mudcake on the wellbore wall.
Not many details on the putative mode of action of FIPs have been published, other than that FIP-fve appeared to stimulate IFN-γ production in human PBMCs via p38-MAPK activation [ 71].
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