Netta AvnoonÂÂ
doi : 10.1038/s41585-022-00656-4
Volume 19 Issue 12, December 2022
Alessandro MorlaccoMarta Biancoand Fabrizio DalMoro
Louise StoneÂÂ
Maria Chiara MasoneÂÂ
Maria Chiara MasoneÂÂ
Maria Chiara MasoneÂÂ
Aaron W. Miller, Kristina L. Penniston, Kate Fitzpatrick, Jos?© Agudelo, Gregory Tasian & Dirk LangeA
doi : 10.1038/s41585-022-00647-5
Kidney stone disease affects ~10% of the global population and the incidence continues to rise owing to the associated global increase in the incidence of medical conditions associated with kidney stone disease including, for example, those comprising the metabolic syndrome. Considering that the intestinal microbiome has a substantial influence on host metabolism, that evidence has suggested that the intestinal microbiome might have a role in maintaining oxalate homeostasis and kidney stone disease is unsurprising. In addition, the discovery that urine is not sterile but, like other sites of the human body, harbours commensal bacterial species that collectively form a urinary microbiome, is an additional factor that might influence the induction of crystal formation and stone growth directly in the kidney. Collectively, the microbiomes of the host could influence kidney stone disease at multiple levels, including intestinal oxalate absorption and direct crystal formation in the kidneys.
Claire M. de la Calle, Kevin Shee, Heiko Yang, Peter E. Lonergan & Hao G. NguyenA
doi : 10.1038/s41585-022-00649-3
In order to proliferate in unfavourable conditions, cancer cells can take advantage of the naturally occurring endoplasmic reticulum-associated unfolded protein response (UPR) via three highly conserved signalling arms: IRE1α, PERK and ATF6. All three arms of the UPR have key roles in every step of tumour progression: from cancer initiation to tumour growth, invasion, metastasis and resistance to therapy.
Nathan D. Burke, Brett Nixon, Shaun D. Roman, John E. Schjenken, Jessica L. H. Walters, R. John Aitken & Elizabeth G. BromfieldA
doi : 10.1038/s41585-022-00640-y
Over the past decade, mounting evidence has shown an alarming association between male subfertility and poor somatic health, with substantial evidence supporting the increased incidence of oncological disease, cardiovascular disease, metabolic disorders and autoimmune diseases in men who have previously received a subfertility diagnosis. This paradigm is concerning, but might also provide a novel window for a crucial health reform in which the infertile phenotype could serve as an indication of potential pathological conditions.
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