Design a small enclosure lid for me: 90 mm long, 60 mm wide, …

Design a small enclosure lid for me: 90 mm long, 60 mm wide, 2 mm thick, corners rounded 4 mm, with four 2.8 mm screw holes 6.5 mm in from each edge and a 20 x 8 mm rectangular cutout in the centre for a display. I use Fusion 360.

Reasoning

I’ll model the lid with a centered origin: the outer dimensions are 90 × 60 mm, holes are through-holes located 6.5 mm from each edge, and the display opening is centered.

Part · built to dimension · millimetres

90 × 60 mm rounded enclosure lid with display cutout

Loading the geometry kernel…

Centered-origin lid: X spans −45 to +45 mm, Y spans −30 to +30 mm, and Z=0 is the underside. The four 2.8 mm through-holes are centred at ±38.5 mm, ±23.5 mm; the 20 × 8 mm display opening is centred and square-cornered.

The 90 × 60 mm rounded enclosure lid with display cutout is ready.

Overall size: 90 × 60 × 2 mm
Corner radius: 4 mm
Screw holes: 4 × Ø2.8 mm through-holes
Hole placement: 6.5 mm from each outer edge
Display opening: centered, 20 × 8 mm, through-cut
Origin: centered on the lid; underside at Z = 0

For Fusion 360, download the STEP file. STL is suitable for printing, and SVG provides drawing views.

Separate question: what did the SELECT trial (semaglutide, 2023) find for major adverse cardiovascular events in people with obesity but without diabetes? Give the hazard ratio and cite the primary paper.

Let me re-check the earlier design work against your spec, then pull the SELECT trial's primary result.

The earlier lid part looks correct against your dimensions, so no changes are needed there. Now let me retrieve the SELECT trial primary paper.

Let me pull the exact hazard ratio and confidence interval from the primary paper's full text.

The scoped full-text search returned nothing quotable (NEJM licensing). Let me read the abstract directly from the PubMed record.

PubMed's page is gated. Let me try the Europe PMC record, which carries the structured abstract with the results figures.

Let me try the Europe PMC REST API, which returns the structured abstract directly.

I have the primary result directly from the structured abstract.

SELECT trial — primary MACE result

In the SELECT trial (Lincoff et al., NEJM 2023; NCT03574597), once-weekly subcutaneous semaglutide 2.4 mg reduced major adverse cardiovascular events in adults with overweight/obesity and established cardiovascular disease but without diabetes:

Hazard ratio: 0.80 (95% CI 0.72–0.90; P < 0.001) for the primary composite endpoint — a ~20% relative risk reduction. A primary cardiovascular end-point event occurred in 569 of the 8803 patients (6.5%) in the semaglutide group and in 701 of the 8801 patients (8.0%) in the placebo group (hazard ratio, 0.80; 95% confidence interval, 0.72 to 0.90; P<0.001).

Trial details for context

Primary endpoint: composite of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke in a time-to-first-event analysis.
Population: patients 45 years of age or older who had preexisting cardiovascular disease and a body-mass index of 27 or greater but no history of diabetes, randomized 1:1 to semaglutide 2.4 mg weekly or placebo.
Size and follow-up: A total of 17,604 patients were enrolled; 8803 were assigned to receive semaglutide and 8801 to receive placebo. The mean duration of follow-up was 39.8±9.4 months.
Tolerability caveat: Adverse events leading to permanent discontinuation of the trial product occurred in 1461 patients (16.6%) in the semaglutide group and 718 patients (8.2%) in the placebo group (P<0.001).

Primary citation

Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. New England Journal of Medicine 2023;389(24):2221–2232. DOI: 10.1056/NEJMoa2307563 (PMID 37952131). PUBMED 37952131

This figure is grounded in the full structured abstract from the primary NEJM paper (retrieved via the Europe PMC record); the exact HR, CI, and P value appear in the Results text quoted above. This is research context, not medical advice.

New topic. In two short paragraphs with citations: what is the current evidence that GLP-1 receptor agonists reduce alcohol consumption in humans? Name the strongest trial.

GLP-1 receptor agonists — semaglutide in particular — reduce some alcohol-consumption outcomes in humans, but the randomized evidence is still early and concentrated in patients with comorbid obesity. The strongest single trial is the Copenhagen SEMALCO trial (Klausen et al., Lancet 2026), which randomized 108 treatment-seeking participants with moderate-to-severe alcohol use disorder (AUD) and comorbid obesity 1:1 to once-weekly subcutaneous semaglutide 2.4 mg or placebo, both added to cognitive behavioural therapy, over 26 weeks. On its primary endpoint, semaglutide reduced heavy drinking days by an estimated 13.7 percentage points more than placebo (95% CI −22.0 to −5.4; p=0.0015), with supporting effects on several secondary alcohol-related outcomes PUBMED 42070571. This is the most robust randomized result to date, but it is critical that the population was specifically obesity-comorbid AUD, so it does not by itself establish efficacy in general (non-obese) AUD. An earlier US phase 2 trial (Hendershot et al., JAMA Psychiatry 2025; n=48, 9 weeks) found that low-dose semaglutide reduced laboratory alcohol self-administration, weekly craving, and drinks per drinking day, but did not change drinks per calendar day or number of drinking days — a directionally supportive but mixed result PUBMED 39937469.

The broader evidence base is consistent but preliminary and mostly non-definitive. A systematic review of three RCTs reported that semaglutide reduced alcohol use and dulaglutide lowered intake in current drinkers, while an exenatide trial found no significant effect on heavy drinking days (with benefit only in a higher-BMI subgroup) PUBMED 41273789 PUBMED 36066977. Observational/pharmacoepidemiology cohorts associate GLP-1RAs with lower alcohol-related hospitalization, but these are vulnerable to confounding by indication and reverse causation and cannot establish causality on their own DOI 10.1002/pu.31274. Taken together, the main caveats are small samples, short follow-up, enrichment for obesity, and gastrointestinal side effects; larger, longer trials in general AUD populations are needed before GLP-1RAs can be considered established AUD therapy. This is research context, not medical advice.

Research session

SELECT trial — primary MACE result

Trial details for context

Primary citation