A pilot randomised controlled trial exploring the feasibility and efficacy of a human-AI sleep coaching model for improving sleep among university students.

Objective: Sleep quality is a crucial concern, particularly among youth. The integration of health coaching with question-answering (QA) systems presents the potential to foster behavioural changes and enhance health outcomes. This study proposes a novel human-AI sleep coaching model, combining health coaching by peers and a QA system, and assesses its feasibility and efficacy in improving university students' sleep quality. Methods: In a four-week unblinded pilot randomised controlled trial, 59 university students (mean age: 21.9; 64% males) were randomly assigned to the intervention (health coaching and QA system; n = 30) or the control conditions (QA system; n = 29). Outcomes included efficacy of the intervention on sleep quality (Pittsburgh Sleep Quality Index; PSQI), objective and self-reported sleep measures (obtained from Fitbit and sleep diaries) and feasibility of the study procedures and the intervention. Results: Analysis revealed no significant differences in sleep quality (PSQI) between intervention and control groups (adjusted mean difference = -0.51, 95% CI: [-1.55-0.77], p = 0.40). The intervention group demonstrated significant improvements in Fitbit measures of total sleep time (adjusted mean difference = 32.5, 95% CI: [5.9-59.1], p = 0.02) and time in bed (adjusted mean difference = 32.3, 95% CI: [2.7-61.9], p = 0.03) compared to the control group, although other sleep measures were insignificant. Adherence was high, with the majority of the intervention group attending all health coaching sessions. Most participants completed baseline and post-intervention self-report measures, all diary entries, and consistently wore Fitbits during sleep. Conclusions: The proposed model showed improvements in specific sleep measures for university students and the feasibility of the study procedures and intervention. Future research may extend the intervention period to see substantive sleep quality improvements.

Can Computerized Simulation be Used to Assess Surgical Proficiency in Laparoscopic Colorectal Surgeries? A Systematic Review.

INTRODUCTION: Computerized simulation (CS) of surgery in virtual reality (VR), augmented reality (AR) and mixed reality (MR) settings are used to teach foundational skills, but its applicability in advanced training is to be determined. This review aims to summarize the types of CS available for laparoscopic colorectal surgery (CRS) and its utility in assessment of proficiency. METHODS: A systematic review of CS in laparoscopic CRS was done on PubMed, Embase, Scopus and Cochrane Library databases. RESULTS: Eleven relevant observational studies were identified. The most common procedure simulated was laparoscopic colectomy. Assessment using performance metrics measured by the simulator such as path length moved by laparoscopic tools, procedure time and number of discrete movements had the most consistent differentiating ability between expert and non-expert cohorts. Surgeons fared similarly in proficiency scores in assessment with CS compared to assessment with traditional cadaveric or porcine models. CONCLUSION: CS of laparoscopic CRS may be used in assessment of proficiency using performance metrics measuring economy of movement. CS may be a viable assessment tool in advanced surgical training, but further studies should assess utility of incorporating it as a formal assessment tool in training programs.

The protective effect of beta-hydroxybutyric acid on renal glomerular epithelial cells in adriamycin-induced injury.

Beta-hydroxybutyric acid (BHB) exerts a protective effect in experimental of kidney disease models. However, the mechanisms underlying this activity are not well defined. BHB stands out for its ability to inhibit the Nε-lysine acetylation of histone and non-histone proteins, which may affect cellular processes and protein functions. In adriamycin-injured murine glomerular podocytes, BHB ameliorates podocyte damage and preserves actin cytoskeleton integrity, reminiscent of the effect of MS275, a highly selective inhibitor of lysine deacetylase. Further research found that adriamycin causes the reduced acetylation of nephrin, WT-1, and GSK3ß. This process is abrogated by the lysine deacetylase inhibitor or BHB, suggesting that the acetylation of these molecules regulates their activity. In contrast, anacardic acid, a selective inhibitor of acetyltransferase, decreases the acetylation of nephrin, WT-1, and GSK3ß and mitigates the podocyte protective effects of BHB. Taken together, BHB attenuates adriamycin-elicited glomerular epithelial cell injury, at least in part, by inhibiting the deacetylation of the key molecules implicated in glomerular injury.

Two conserved epigenetic regulators prevent healthy ageing.

It has long been assumed that lifespan and healthspan correlate strongly, yet the two can be clearly dissociated1-6. Although there has been a global increase in human life expectancy, increasing longevity is rarely accompanied by an extended healthspan4,7. Thus, understanding the origin of healthy behaviours in old people remains an important and challenging task. Here we report a conserved epigenetic mechanism underlying healthy ageing. Through genome-wide RNA-interference-based screening of genes that regulate behavioural deterioration in ageing Caenorhabditis elegans, we identify 59 genes as potential modulators of the rate of age-related behavioural deterioration. Among these modulators, we found that a neuronal epigenetic reader, BAZ-2, and a neuronal histone 3 lysine 9 methyltransferase, SET-6, accelerate behavioural deterioration in C. elegans by reducing mitochondrial function, repressing the expression of nuclear-encoded mitochondrial proteins. This mechanism is conserved in cultured mouse neurons and human cells. Examination of human databases8,9 shows that expression of the human orthologues of these C. elegans regulators, BAZ2B and EHMT1, in the frontal cortex increases with age and correlates positively with the progression of Alzheimer's disease. Furthermore, ablation of Baz2b, the mouse orthologue of BAZ-2, attenuates age-dependent body-weight gain and prevents cognitive decline in ageing mice. Thus our genome-wide RNA-interference screen in C. elegans has unravelled conserved epigenetic negative regulators of ageing, suggesting possible ways to achieve healthy ageing.

The use of remifentanil in critically ill patients undergoing percutaneous dilatational tracheostomy: A prospective randomized-controlled trial.

Remifentanil was a µ-agonist, with a rapid onset, a powerful narcotic analgesic activity and a fast nonspecific esterases hydrolyzation and theoretically an ideal opioid for percutaneous dilatational tracheostomy (PDT). The present study discussed use of remifentanil in critically ill patients undergoing PDT. Ninety-nine patients were randomly assigned to the propofol/remifentanil group (PR group, n = 49) or the propofol group (P group, n = 50). Two patients (one in P group and one in PR group) were excluded and transferred to surgical way of tracheostomy because of uncontrolled bleeding. The primary outcomes were critical care pain observation (CPOT) scores during PDT; hemodynamic response and side effects, such as bleeding and muscle rigidity (MR). CPOT scores in P group were significantly higher than in PR group during incision and dilation stages (P < 0.05 and P < 0.01). Systolic blood pressure had a significant drop after a bolus of remifentanil in PR group compared with patients in P group (P < 0.056). The incidence of MR was significantly higher in PR group than in P group (P < 0.05). Recovery time in PR group was significantly shorter than in P group (P < 0.05). The occurrence of tachycardia, bleeding, vomiting, and nausea had no statistically differences in both groups. Patients in PR group were undergoing shorter recovery time and better experience of pain in PDT compared with patients in P group, but MR seemed to be higher in PR group. Remifentanil seemed to be a safe and effective opioid used in critically ill patients undergoing PDT.

Novel function of PIWIL1 in neuronal polarization and migration via regulation of microtubule-associated proteins.

BACKGROUND: Young neurons in the developing brain establish a polarized morphology for proper migration. The PIWI family of piRNA processing proteins are considered to be restrictively expressed in germline tissues and several types of cancer cells. They play important roles in spermatogenesis, stem cell maintenance, piRNA biogenesis, and transposon silencing. Interestingly a recent study showed that de novo mutations of PIWI family members are strongly associated with autism. RESULTS: Here, we report that PIWI-like 1 (PIWIL1), a PIWI family member known to be essential for the transition of round spermatid into elongated spermatid, plays a role in the polarization and radial migration of newborn neurons in the developing cerebral cortex. Knocking down PIWIL1 in newborn cortical neurons by in utero electroporation of specific siRNAs resulted in retardation of the transition of neurons from the multipolar stage to the bipolar stage followed by a defect in their radial migration to the proper destination. Domain analysis showed that both the RNA binding PAZ domain and the RNA processing PIWI domain in PIWIL1 were indispensable for its function in neuronal migration. Furthermore, we found that PIWIL1 unexpectedly regulates the expression of microtubule-associated proteins in cortical neurons. CONCLUSIONS: PIWIL1 regulates neuronal polarization and radial migration partly via modulating the expression of microtubule-associated proteins (MAPs). Our finding of PIWIL1's function in neuronal development implies conserved functions of molecules participating in morphogenesis of brain and germline tissue and provides a mechanism as to how mutations of PIWI may be associated with autism.