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Qaagi - Book of Why

Causes

Effects

Antibody inhibition of KHC in human fibroblasts and gene disruption in mousecausesextraembryonic cells

squamous cellsresultingin clue cells

TLE1 ( Fig . 4C and Fig(passive) caused byPax6-expressig cells

orderto createelastin cells

within the vaginal discharge of patients with bacterial vaginosis G. Symptoms of vaginal burning , pruritus , discharge , bleeding , and dyspareunia in postmenopausal girls(passive) are discoveredClue cells

basal(passive) led byhypodermal cells

formation of AlP , which is a factorcauseseutectic cells

a defective iron carrier ( 4 - 7(passive) caused byerythoid cells

the above - described formation of AlP(passive) caused byeutectic cells

from three state-1 neighbours(passive) are created--State-3 cells

pressure exerted on the chest wall at the outset of systole by the rounded and hardened ventricular wall(passive) is caused bypacemaking cells

this Philo mixing developing a active access or usecould contributethis Philo mixing developing a active access or use

in loss of experimental material and invalid experimental resultsresultingin loss of experimental material and invalid experimental results

Mitotic arrest in wild - type megakaryocytes treated with Plk1 inhibitors or(passive) is triggeredMitotic arrest in wild - type megakaryocytes treated with Plk1 inhibitors or

for optimum photovoltaic responsedesignedfor optimum photovoltaic response

up to 80 or 90 per cent of the overall phytoplankton communitymay contributeup to 80 or 90 per cent of the overall phytoplankton community

in ‘ indirect contamination ’ of the 32,755 articles based on them , plus the estimated half a million other papers which cited these cellsresultedin ‘ indirect contamination ’ of the 32,755 articles based on them , plus the estimated half a million other papers which cited these cells

even after pretreatment with 5-AZA - dC ( 200 nmol / L ) over 4 daysresultedeven after pretreatment with 5-AZA - dC ( 200 nmol / L ) over 4 days

MET amplification upon resistance to an EGFR TKI did n’t undergo an EMThad createdMET amplification upon resistance to an EGFR TKI did n’t undergo an EMT

MET amplification upon resistance to an EGFR TKI did not undergo an EMThad createdMET amplification upon resistance to an EGFR TKI did not undergo an EMT

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