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OTC 303-1633 Roller 最高 Rocker Follower Remover 即出荷 EcoBoost V8 for Ti-VCT Ford

OTC 303-1633 Roller Rocker Follower Remover for Ford EcoBoost Ti-VCT V8

$96

OTC 303-1633 Roller Rocker Follower Remover for Ford EcoBoost Ti-VCT V8

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Item specifics

Condition:
New
Manufacturer Part Number:
303-1633
Brand:
OTC
UPC:
Does not apply

OTC 303-1633 Roller Rocker Follower Remover for Ford EcoBoost Ti-VCT V8

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a leading international journal from BMJ and BSG, publishes cutting-edge gastroenterology and hepatology research and reviews

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Gut is a Plan S compliant Transformative Journal.

Gut is a leading international journal in gastroenterology and hepatology and has an established reputation for publishing first class clinical research of the alimentary tract, the liver, biliary tree and pancreas. Gut delivers up-to-date, authoritative, clinically oriented coverage in all areas of gastroenterology and hepatology. Regular features include articles by leading authorities describing novel mechanisms of disease and new management strategies, both diagnostic and therapeutic, likely to impact on clinical practice within the foreseeable future.

Gut is an official journal of the British Society of Gastroenterology and has two companion titles: Frontline Gastroenterology for education and practice and BMJ Open Gastroenterology for sound science clinical research.

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Our new online collection highlights all research relating to the COVID-19 pandemic published by Gut, Frontline Gastroenterology and BMJ Open Gastroenterology. It is updated regularly as new articles are published.

 

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Synergistic targeting and resistance to PARP inhibition in pancreatic cancer

To cite: Gout J, Perkhofer L, Morawe M, et al. Gut 2021;70:743-760.

Read the full article here: link
Objective: ATM serine/threonine kinase (ATM) is the most frequently mutated DNA damage response gene, involved in homologous recombination (HR), in pancreatic ductal adenocarcinoma (PDAC).

Conclusion: Analysis of the molecular susceptibilities triggered by ATM deficiency in PDAC allow elaboration of an efficient mutation-specific combinational therapeutic approach that can be also implemented in a genotype-independent manner by ATM inhibition.

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