Chan-Chuang qigong with breathing meditation improves quality of life and interoceptive awareness in patients with breast cancer: a randomised controlled trial.

PURPOSE: To evaluate the effect of Chan-Chuang qigong with breathing meditation on quality of life (QoL) and interoceptive awareness in patients with breast cancer during chemotherapy. METHODS: This was a randomised controlled trial. Participants were randomly assigned to a qigong group (n = 30), which practised Chan-Chuang qigong with breathing meditation for 15 weeks, and a control group (n = 30), which received routine care. Outcomes were measured by using the European Organization for Research and Treatment of Cancer QoL Questionnaire (EORTC QLQ-C30) and Multidimensional Assessment of Interoceptive Awareness (MAIA-C). RESULTS: The qigong group, when compared with the control group and baseline, exhibited significantly improved emotional function (p = 0.01) and decreased role function (p = 0.04) at week 15. The MAIA-C indicated a significant difference between groups in self-regulation at week 15 (p = 0.04). Within the qigong group, changes were found in attention regulation (p = 0.03), emotional awareness (p = 0.04), self-regulation (p = 0.01), and body listening (p = 0.002). CONCLUSIONS: A 15-week programme of Chan-Chuang qigong with breathing meditation is a simple and safe intervention for patients with breast cancer to improve their emotional function and adjust to their role identity. Participants who practised qigong achieved increased awareness of their own bodies and were able to better regulate their emotion and attention. TRIAL REGISTER: ClinicalTrials.gov Identifier: NCT05385146.

DROIDS 1.20: A GUI-Based Pipeline for GPU-Accelerated Comparative Protein Dynamics.

Traditional informatics in comparative genomics work only with static representations of biomolecules (i.e., sequence and structure), thereby ignoring the molecular dynamics (MD) of proteins that define function in the cell. A comparative approach applied to MD would connect this very short timescale process, defined in femtoseconds, to one of the longest in the universe: molecular evolution measured in millions of years. Here, we leverage advances in graphics-processing-unit-accelerated MD simulation software to develop a comparative method of MD analysis and visualization that can be applied to any two homologous Protein Data Bank structures. Our open-source pipeline, DROIDS (Detecting Relative Outlier Impacts in Dynamic Simulations), works in conjunction with existing molecular modeling software to convert any Linux gaming personal computer into a "comparative computational microscope" for observing the biophysical effects of mutations and other chemical changes in proteins. DROIDS implements structural alignment and Benjamini-Hochberg-corrected Kolmogorov-Smirnov statistics to compare nanosecond-scale atom bond fluctuations on the protein backbone, color mapping the significant differences identified in protein MD with single-amino-acid resolution. DROIDS is simple to use, incorporating graphical user interface control for Amber16 MD simulations, cpptraj analysis, and the final statistical and visual representations in R graphics and UCSF Chimera. We demonstrate that DROIDS can be utilized to visually investigate molecular evolution and disease-related functional changes in MD due to genetic mutation and epigenetic modification. DROIDS can also be used to potentially investigate binding interactions of pharmaceuticals, toxins, or other biomolecules in a functional evolutionary context as well.

A Novel Neuroprotective Small Molecule for Glial Cell Derived Neurotrophic Factor Induction and Photoreceptor Rescue.

PURPOSE: Degenerative diseases of the retina, such as retinitis pigmentosa and age-related macular degeneration, are characterized by the irreversible loss of photoreceptors. Several growth factors, including glial cell derived neurotrophic factor (GDNF), have been shown to rescue retinal neurons. An alternative strategy to direct GDNF administration is its induction in host retina by small molecules. Here we studied the ability of a novel small molecule GSK812 to induce GDNF in vitro/in vivo and rescue photoreceptors. METHODS: GDNF induction in vitro was assessed in human ARPE-19, human retinal progenitor cells (RPCs) and mouse pluripotent cell-derived eyecups. For time course pharmacokinetic and GDNF induction studies in C57Bl/6 mice, GSK812 sustained release formulation was injected intravitreally. The same delivery approach was used in the rhodopsin knockout mice and Royal College of Surgeon (RCS) rats to assess long-term GDNF induction and photoreceptor rescue. RESULTS: The suspension provided sustained GSK812 delivery with 28 µg of drug remaining in the eye 2 weeks after a single injection. GSK812 suspension injection in C57Bl/6 mice resulted in significant upregulation of GDNF mRNA (>1.8-fold) and protein levels (>2.8-fold). Importantly, GSK812 treatment resulted in outer nuclear layer preservation in rho-/- mice with a 2-fold difference in photoreceptor number. In the RCS rat, the GSK812 injection provided long-term rescue of photoreceptors and outer segments, accompanied by function preservation as well. CONCLUSIONS: GSK812 is a potent neuroprotectant that can induce GDNF in normal and diseased retina. This induction results in photoreceptor rescue in 2 models of retinal degeneration.