Environmental genomics can describe all forms of organisms—cellular and viral—present in a community. The analysis of such eco-systems biology data relies heavily on reference databases, e.g., taxonomy or gene function databases. Reference databases of symbiosis sensu lato, although essential for the analysis of organism interaction networks, are lacking. By mining existing databases and literature, we here provide a comprehensive and manually curated database of taxonomic links between viruses and their cellular hosts.

The aim of this study was to elucidate the ecological structure of the human gut temperate bacteriophage community and its role in inflammatory bowel disease (IBD). Temperate bacteriophages make up a large proportion of the human gut microbiota and are likely to play a role in IBD pathogenesis. However, many of these bacteriophages await characterization in reference databases. Therefore, we conducted a large-scale reconstruction of temperate bacteriophage and bacterial genomes from the whole-metagenome sequence data generated by the IBD Multi’omics Database project. By associating phages with their hosts via genome comparisons, we found that temperate bacteriophages infect a phylogenetically wide range of bacteria. The majority of variance in bacteriophage community composition was explained by variation among individuals, but differences in the abundance of temperate bacteriophages were identified between IBD and non-IBD patients. Of note, in active ulcerative colitis patients, temperate bacteriophages infecting Bacteroides uniformis and Bacteroides thetaiotaomicron—two species experimentally proven to be beneficial to gut homeostasis—were over-represented, whereas their hosts were under-represented in comparison with non-IBD patients. Supporting the mounting evidence that gut viral community plays a vital role in IBD, our results show potential association between temperate bacteriophages and IBD pathogenesis.

Background: Cardiac rehabilitation (CR) is effective in preventing cardiovascular diseases; however, participation in CR programs remains limited due to the associated challenges. The integration of wearable devices and real-time monitoring offers a potential solution to enhance adherence to remote CR programs and their outcomes. Objective: This study aimed to evaluate the efficacy of a remote CR program using wearable devices and real-time monitoring with or without online coaching (OLC) in improving exercise capacity in patients with coronary artery disease (CAD). Methods: We enrolled 50 patients with CAD in a remote CR program in this randomized, open-label, single-center pilot trial (phase III). After baseline cardiopulmonary exercise tests (CPETs), all patients were assigned a CPET-based home exercise program and were provided with a wearable device (Fitbit Sense; Fitbit, Inc) with a real-time monitoring system (Recoval; SapplyM, Inc). The patients were randomly assigned to an intervention group with OLC (n=25) or a control wearable device (CON; n=25) group. The primary outcomes were changes in peak oxygen consumption (peak VO₂) and anaerobic threshold VO₂ (oxygen consumption) at 12 weeks. The secondary outcomes were changes in CPET parameters, daily activity, anxiety levels, and health-related quality of life. Results: Peak VO₂ and anaerobic threshold VO₂ increased significantly from baseline to 12 weeks in the OLC (+1.6 mL/kg/min, P<.001; +1.0 mL/kg/min, P=.001) and CON (+0.6 mL/kg/min, P=.008; +1.3 mL/kg/min, P=.002) groups with no significant between-group differences (P=.65 and P=.90). In the latter half of the intervention, the daily distance and highly active time in the OLC group were significantly increased compared with those in the CON group (all P<.05). Mental status and health-related quality of life scores showed no significant differences between the groups. No major adverse cardiac events were reported. One patient in the OLC group dropped out due to lower limb muscle strain. Conclusions: Remote CR using wearable devices and a real-time monitoring system significantly improved exercise capacity in patients with CAD over a 12-week intervention program. The addition of regular OLC to the intervention program further enhanced the physical activity levels, particularly in high-intensity activities. Future studies are warranted to validate these findings in more diverse populations and over longer intervention periods to optimize the benefits and safety of remote CR programs.

Purpose Asians often face the problems of clopidogrel resistance and East Asian paradox. This study aimed to evaluate the effects of P2Y₁₂ inhibitors, including low-dose prasugrel 2.5 mg, on the P2Y₁₂ reaction unit (PRU) in the chronic phase after percutaneous coronary intervention (PCI). Methods A total of 348 patients were studied. PRU was measured 6–12 months after PCI and subsequently, 6 months later using a P2Y₁₂ assay, respectively. This study evaluated the proportion of bleeding risk (PRU ≤ 85) and ischemic risk (PRU ≥ 239) as primary endpoints, and the prediction of bleeding risk and ischemic risk using multivariable logistic regression analysis. Results At baseline, 136 patients (39%) received prasugrel 3.75 mg, 48 patients (14%) received prasugrel 2.5 mg, and 164 patients (47%) received clopidogrel 75 mg. Clopidogrel 75 mg had a significantly higher proportion of ischemic risk within one year after PCI than the other groups, and was an independent predictor for ischemic risk with reference of prasugrel 3.75 mg. In addition, switching from clopidogrel 75 mg to prasugrel 2.5 mg significantly lowered and aggregated the PRU value. Whereas, dose reduction of prasugrel had a significantly lower proportion of bleeding risk over one year after PCI than the continuation of prasugrel 3.75 mg, and was an independent predictor for bleeding risk with reference of continuation of prasugrel 3.75 mg. Conclusions Prasugrel 2.5 mg has a lower ischemic risk and a more stable PRU value compared with clopidogrel treatment. Prasugrel also contributes to a decline in bleeding risk with concomitant dose reduction. Trial Registration University Hospital Medical Information Network (UMIN), ID: UMIN000029541, Date: October 16, 2017 (https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000033395).

Background: Gankyrin (GK) is an oncoprotein which regulates inflammatory responses and its inhibition is considered as a possible anti-inflammatory therapy for inflammatory bowel disease (IBD). Methods: In this study, we investigated the role of GK in epithelial cells using mice with intestinal epithelial cell-specific GK deletion in (i) the entire small intestine and colon (Villin-Cre;Gankyrin^f/f) and (ii) the distal intestine and colon (Cdx2-Cre;Gankyrin^f/f). Result: Unexpectedly, GK-deficiency in the upper small bowel augmented inflammatory activity compared with control mice when colitis was induced with dextran sodium sulfate. Biochemical analyses have revealed GK-deficiency to have caused reduction in the expression of antimicrobial peptides, α-Defensin-5 and -6, in the upper small bowel. Examination of human samples have further confirmed that the reduction of GK expression in the small bowel is associated with colonic involvement in human Crohn’s disease. Through the sequencing of bacterial 16S rRNA gene amplicons, bacteria potentially deleterious to intestinal homeostasis such as Helicobacter japonicum and Bilophila were found to be over-represented in colitis induced Villin-Cre;Gankyrin^f/f mice when compared to Gankyrin^f/f control mice under the same condition. Conclusion: These results highlight the distinct site dependence of the pro- and anti-inflammatory functions of GK and provide important insights into the pathogenesis of IBD.