Clinical prediction models are increasingly deployed to support diagnostic and prognostic decisions, making reproducibility essential for assessing their reliability and generalizability. Analytical code supports independent assessment of these processes, yet its availability in the literature remains limited. This scoping review quantifies current practices in sharing analytical code to inform the development of TRIPOD-Code, a reporting guideline for code availability and reproducibility. Here a large-language-model-assisted pipeline was developed to screen articles citing TRIPOD or TRIPOD+AI, extract repository links and assess retrieved repositories against 14 predefined reproducibility-related features. Among 3,967 articles, 482 (12.2%) included code-sharing statements. Sharing prevalence varied widely by journal and country. Repository assessment showed substantial heterogeneity in reproducibility features. These findings underscore the need for clearer expectations beyond code availability, including documentation, dependency specification and executable structure. Strengthening these practices may improve the usability of clinical prediction model studies and support their deployment in real-world clinical settings. An analysis of code availability in the open-access published literature shows that code sharing in clinical prediction models remains limited and reveals significant variability in practices and documentation quality.
The International Consortium of Digital Twins in Healthcare and Medicine was established to advance medical digital twin technology as a new infrastructure for precision health.
Alzheimer’s disease (AD) is conventionally framed as a consequence of progressive amyloid-β and tau pathology, yet substantial heterogeneity in cognitive outcome at any given level of pathological burden indicates that cognitive resilience constitutes a parallel determinant of disease risk. Here we test whether pathology and resilience function as independent and synergistic dimensions of incident AD dementia. In 3,119 older adults from the China Cognition and Aging Study, followed for a median of 13.7 years, we derived two longitudinal indices from repeated measurements: a pathology score indexed by tau phosphorylated at threonine 181/amyloid-β42, and a cognitive resilience score defined as the residual of the cognitive slope after adjustment for pathology, age and sex. Both indices independently predicted incident AD dementia (pathology: hazard ratio 2.50 per s.d., 95% confidence interval 2.30–2.72; resilience: hazard ratio 0.51 per s.d., 95% confidence interval 0.48–0.55). The two dimensions contributed comparable, complementary shares of 10-year AD risk and together captured substantially more of the explainable risk than either dimension alone. They also interacted multiplicatively: the lowest risk of incident AD was observed in individuals with both high resilience and low pathology, whereas the highest risk occurred in those with both high pathology and low resilience. Findings were replicated in an independent cohort and were robust in reverse-causation sensitivity analyses. These findings broaden the understanding that AD dementia is shaped jointly by pathological burden and cognitive resilience, and argue for therapeutic trial and prevention strategies that strengthen resilience alongside reducing pathology. ClinicalTrials.gov registration: NCT03653156 . A 15-year cohort study shows that Alzheimer’s dementia risk is jointly shaped by Alzheimer’s pathology and cognitive resilience, with high resilience linked to lower risk, even under greater pathology.
Teclistamab, a B cell maturation antigen-targeting bispecific antibody, has demonstrated substantial activity in relapsed multiple myeloma (MM), particularly in earlier lines of therapy, and may have higher efficacy in high-risk smoldering MM (HR-SMM) with a more functional immune system. In the randomized phase 2 ImmunoPRISM trial, we compared fixed-duration teclistamab with lenalidomide–dexamethasone (Rd) in HR-SMM. After a six-patient safety run-in, patients were randomized 2:1 to teclistamab or Rd. The primary endpoint was complete response (CR) rate. As of 26 May 2026, 59 patients were treated—45 received teclistamab and 14 received Rd. Teclistamab treatment induced a CR in 77.8% patients versus 0% with Rd, and minimal residual disease negativity at 10−5 in 82.2% patients. At a median follow-up of 24.5 months, 2-year progression-free survival was 92% with teclistamab versus 49% with Rd. Overall, response rates, duration of response and time to progression (TTP) were significantly improved in teclistamab compared to Rd. Toxicities in the teclistamab arm included grades 1–2 cytokine release syndrome, no neurotoxicity and no increase in grade 3 infections compared to Rd (20% versus 21%). No deaths occurred in either arm. Teclistamab represents a highly active immune-interception strategy for HR-SMM. ClinicalTrials.gov registration: NCT05469893 . In the randomized phase 2 ImmunoPRISM trial, patients with high-risk smoldering multiple myeloma (MM) showed higher rates of complete clinical responses in response to treatment with teclistamab compared with lenalidomide–dexamethasone, although longer follow-up is required to determine durable prevention of progression to MM.
