The carbon footprint of ambulatory gastrointestinal endoscopy.

BACKGROUND: Endoscopy is considered the third highest generator of waste within healthcare. This is of public importance as approximately 18 million endoscopy procedures are performed yearly in the USA and 2 million in France. However, a precise measure of the carbon footprint of gastrointestinal endoscopy (GIE) is lacking. METHODS: This retrospective study for 2021 was conducted in an ambulatory GIE center in France where 8524 procedures were performed on 6070 patients. The annual carbon footprint of GIE was calculated using "Bilan Carbone" of the French Environment and Energy Management Agency. This multi-criteria method accounts for direct and indirect greenhouse gas (GHG) emissions from energy consumption (gas and electricity), medical gases, medical and non-medical equipment, consumables, freight, travel, and waste. RESULTS: GHG emissions in 2021 were estimated to be 241.4 tonnes CO2 equivalent (CO2e) at the center, giving a carbon footprint for one GIE procedure of 28.4 kg CO2e. The main GHG emission, 45 % of total emissions, was from travel by patients and center staff to and from the center. Other emission sources, in rank order, were medical and non-medical equipment (32 %), energy consumption (12 %), consumables (7 %), waste (3 %), freight (0.4 %), and medical gases (0.005 %). CONCLUSIONS: This is the first multi-criteria analysis assessing the carbon footprint of GIE. It highlights that travel, medical equipment, and energy are major sources of impact, with waste being a minor contributor. This study provides an opportunity to raise awareness among gastroenterologists of the carbon footprint of GIE procedures.

The laminin response in inflammatory bowel disease: protection or malignancy?

Laminins (LM), basement membrane molecules and mediators of epithelial-stromal communication, are crucial in tissue homeostasis. Inflammatory Bowel Diseases (IBD) are multifactorial pathologies where the microenvironment and in particular LM play an important yet poorly understood role in tissue maintenance, and in cancer progression which represents an inherent risk of IBD. Here we showed first that in human IBD colonic samples and in murine colitis the LMα1 and LMα5 chains are specifically and ectopically overexpressed with a concomitant nuclear p53 accumulation. Linked to this observation, we provided a mechanism showing that p53 induces LMα1 expression at the promoter level by ChIP analysis and this was confirmed by knockdown in cell transfection experiments. To mimic the human disease, we induced colitis and colitis-associated cancer by chemical treatment (DSS) combined or not with a carcinogen (AOM) in transgenic mice overexpressing LMα1 or LMα5 specifically in the intestine. We demonstrated that high LMα1 or LMα5 expression decreased susceptibility towards experimentally DSS-induced colon inflammation as assessed by histological scoring and decrease of pro-inflammatory cytokines. Yet in a pro-oncogenic context, we showed that LM would favor tumorigenesis as revealed by enhanced tumor lesion formation in both LM transgenic mice. Altogether, our results showed that nuclear p53 and associated overexpression of LMα1 and LMα5 protect tissue from inflammation. But in a mutation setting, the same LM molecules favor progression of IBD into colitis-associated cancer. Our transgenic mice represent attractive new models to acquire knowledge about the paradoxical effect of LM that mediate either tissue reparation or cancer according to the microenvironment. In the early phases of IBD, reinforcing basement membrane stability/organization could be a promising therapeutic approach.

Harms of colonoscopy in a colorectal cancer screening programme with faecal occult blood test: a population-based cohort study.

BACKGROUND AND AIMS: To assess the harms of colonoscopy in a real world colorectal cancer screening programme with faecal occult blood test. METHODS: Retrospective cohort study of all colonoscopies performed in patients aged 50-74 for a positive guaiac-based faecal occult blood test between September 2003 and February 2010 within the screening programme in progress in Alsace (France). Adverse events were recorded through prospective voluntary reporting by gastroenterologists and retrospective postal surveys addressed to persons screened and their general practitioners. RESULTS: Of 10,277 colonoscopies, 250 adverse events were recorded, 48 (4.7 ‰, 95% CI 3.4-6.0) of them being moderate or severe, mainly 10 (1.0 ‰, 95% CI 0.4-1.6) perforations and 31 (3.0 ‰, 95% CI 2.0-4.1) bleeding. 91.7% of moderate and severe adverse events were the result of a therapeutic procedure. Of 103 serious adverse events, eight (7.8%) were considered preventable. Gastroenterologists reported 52.2% of moderate and severe adverse events. A mild adverse event or an incident was reported in up to 97.0 ‰ (95% CI 83.2-110.7) colonoscopies. CONCLUSION: The harms of colonoscopy were underestimated in all randomized controlled trials on colorectal cancer screening with faecal occult blood test. They are greater in a real world programme, estimated at 7.5 major and 100 minor adverse events per 1000 colonoscopies.

Abnormal Wnt and PI3Kinase signaling in the malformed intestine of lama5 deficient mice.

Laminins are major constituents of basement membranes and are essential for tissue homeostasis. Laminin-511 is highly expressed in the intestine and its absence causes severe malformation of the intestine and embryonic lethality. To understand the mechanistic role of laminin-511 in tissue homeostasis, we used RNA profiling of embryonic intestinal tissue of lama5 knockout mice and identified a lama5 specific gene expression signature. By combining cell culture experiments with mediated knockdown approaches, we provide a mechanistic link between laminin α5 gene deficiency and the physiological phenotype. We show that laminin α5 plays a crucial role in both epithelial and mesenchymal cell behavior by inhibiting Wnt and activating PI3K signaling. We conclude that conflicting signals are elicited in the absence of lama5, which alter cell adhesion, migration as well as epithelial and muscle differentiation. Conversely, adhesion to laminin-511 may serve as a potent regulator of known interconnected PI3K/Akt and Wnt signaling pathways. Thus deregulated adhesion to laminin-511 may be instrumental in diseases such as human pathologies of the gut where laminin-511 is abnormally expressed as it is shown here.