Global Literature Analysis of Tumor Organoid and Tumor-on-Chip Research.

: Tumor organoid and tumor-on-chip (ToC) platforms replicate aspects of the anatomical and physiological states of tumors. They, therefore, serve as models for investigating tumor microenvironments, metastasis, and immune interactions, especially for precision drug testing. To map the changing research diversity and focus in this field, we performed a quality-controlled text analysis of categorized academic publications and clinical studies.

Do perilunate dislocations and fracture-dislocations result in different radiological outcomes following wrist alignment reconstruction? A single-center retrospective study including 51 patients with perilunate injuries.

Introduction: Perilunate dislocations (PLD) and perilunate fracture-dislocations (PLFD) are high-energy wrist injuries often linked to significant post-traumatic osteoarthritis. This study aims to determine whether PLD and PLFD yield different radiological outcomes following surgical treatment while identifying prognostic factors for worse outcomes.

Materials And Methods: We retrospectively analyzed 51 patients treated for perilunate injuries between 2000 and 2022.

Acute remote ischemic conditioning enhances (CD3+)- but not (FoxP3+)-T-cell invasion in the tumor center and increases IL 17 and TNF-alpha expression in a murine melanoma model.

Introduction: Hypoxia can drive tumor progression, suppress anti-tumor immunity, and reduce the effectiveness of radiotherapy and chemotherapy. This study aimed to assess the impact of remote ischemic conditioning (RIC) on tumor oxygenation (sO2) and the anti-tumor immune response.

Material And Methods: Fourteen B16-Ova tumor-bearing C57BL/6N mice received six 5-minute RIC cycles, while another fourteen underwent anesthesia only.

Corrigendum: How general is the natural frequency effect? The case of joint probabilities.

[This corrects the article DOI: 10.3389/fpsyg.2024.

A novel aurone RNA CAG binder inhibits the huntingtin RNA-protein interaction.

Huntington's disease (HD) is a devastating, incurable condition whose pathophysiological mechanism relies on mutant RNA CAG repeat expansions. Aberrant recruitment of RNA-binding proteins by mutant CAG hairpins contributes to the progress of neurodegeneration. In this work, we identified a novel binder based on an aurone scaffold that reduces the level of binding of HTT mRNA to the MID1 protein .