You will be shown a scientific claim, and the abstract of a biomedical research paper. Each sentence from the abstract will be on a separate line. Your task is to return a JSON object with two fields:

- "verdict": The fact-checking verdict. If the information in the abstract supports the claim, write "SUPPORT". If the abstract contradicts the claim, write "CONTRADICT". If the abstract does not provide enough information to arrive at a verdict, write "NEI" (for "not enough information").
- "evidence": An array of sentences providing evidence for the verdict. Please copy all relevant sentences verbatim from the abstract. If the verdict was "NEI", then return an empty array.

For instance, if the model were given the claim "smoking causes cancer", the output might be
{
  "verdict": "SUPPORT",
  "evidence": ["The results of our meta-analysis provide overwhelming support that cigarette smoking is a risk cause for lung cancer."]
}

Your response should not include any text other than the json.

Claim: The deregulated and prolonged activation of monocytes improves inflammatory disease outcomes.

Abstract:
RATIONALE Hemizygous deficiency of the transcription factor Krüppel-like factor 2 (KLF2) has been shown previously to augment atherosclerosis in hypercholesterolemic mice.
However, the cell type responsible for the increased atherosclerosis due to KLF2 deficiency has not been identified.
This study examined the consequence of myeloid cell-specific KLF2 inactivation in atherosclerosis.
METHODS AND RESULTS Cell-specific knockout mice were generated by Cre/loxP recombination.
Macrophages isolated from myeloid-specific Klf2 knockout (myeKlf2(-/-)) mice were similar to myeKlf2(+/+) macrophages in response to activation, polarization, and lipid accumulation.
However, in comparison to myeKlf2(+/+) macrophages, myeKlf2(-/-) macrophages adhered more robustly to endothelial cells.
Neutrophils from myeKlf2(-/-) mice also adhered more robustly to endothelial cells, and fewer myeKlf2(-/-) neutrophils survived in culture over a 24-hour period in comparison with myeKlf2(+/+) neutrophils.
When myeKlf2(-/-) mice were mated to Ldlr(-/-) mice and then fed a high fat and high cholesterol diet, significant increase in atherosclerosis was observed in the myeKlf2(-/-)Ldlr(-/-) mice compared with myeKlf2(+/+)Ldlr(-/-) littermates.
The increased atherosclerosis in myeKlf2(-/-)Ldlr(-/-) mice was associated with elevated presence of neutrophils and macrophages, with corresponding increase of myeloperoxidase as well as chlorinated and nitrosylated tyrosine epitopes in their lesion areas compared with myeKlf2(+/+)Ldlr(-/-) mice.
CONCLUSIONS This study documents a role for myeloid KLF2 expression in modulating atherosclerosis.
The increased neutrophil accumulation and atherosclerosis progression with myeloid-specific KLF2 deficiency also underscores the importance of neutrophils in promoting vascular oxidative stress and atherosclerosis.
Collectively, these results suggest that elevating KLF2 expression may be a novel strategy for prevention and treatment of atherosclerosis.
{"verdict": "NEI", "evidence": []}