[The mediating effect of coping style between illness perception and fear of cancer recurrence in patients undergoing radical prostatectomy].

OBJECTIVE: To explore the mediating effect of coping style between illness perception and fear of cancer recurrence in patients undergoing radical prostatectomy. METHODS: A questionnaire survey was carried out in 254 eligible patients who underwent radical prostatectomy in the urology department of two comprehensive tertiary hospitals in Wenzhou City from June 2022 to December 2022. The questionnaires include the general data questionnaire, brief illness perception questionnaire (BIPQ), Medical Coping Modes Questionnaire (MCMQ) and Fear of Progression Questionnaire-Short Form (FoP-Q-SF). A structural equation model was used to analyze the mediating effect of coping style between illness perception and fear of cancer recurrence. RESULTS: The score of fear of cancer recurrence in prostate cancer patients is (30.08 ± 10.11). Illness perception, avoidance, and surrender coping styles could forward prediction fear of cancer recurrence (P=0.001, P=0.019, P=0.001); facing coping styles can negatively predict fear of cancer recurrence (P=0.001). Coping style played a part of the mediating role between illness perception and fear of cancer recurrence, and the mediating effect is 0.150，which accounted for 47.62% of the total effect. CONCLUSION: Coping style is a mediator between illness perception and fear of cancer recurrence in patients undergoing radical prostatectomy. Doctors and nurses should reduce patients' negative perception, guide them to adopt positive coping strategies, and thereby reduce their fear of cancer recurrence.

Integrated Analysis of Key Genes and Pathways Involved in Fetal Growth Restriction and Their Associations With the Dysregulation of the Maternal Immune System.

Fetal growth restriction (FGR) is a common pregnancy complication and a risk factor for infant death. Most patients with FGR have preeclampsia, gestational diabetes mellitus, or other etiologies, making it difficult to determine the specific molecular mechanisms underlying FGR. In this study, an integrated analysis was performed using gene expression profiles obtained from Gene Expression Omnibus. Differentially expressed genes (DEGs) between healthy and FGR groups were screened and evaluated by functional enrichment and network analyses. In total, 80 common DEGs (FDR < 0.05) and 17 significant DEGs (FDR < 0.005) were screened. These genes were enriched for functions in immune system dysregulation in the placenta based on Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Among hub genes identified as candidates for FGR and fetal reprogramming, LEP, GBP5, HLA-DQA1, and CTGF were checked by quantitative polymerase chain reaction, immunohistochemistry, and western blot assays in placental tissues. Immune imbalance could cause hypoxia environment in placenta tissues, thus regulating the fetal-reprogramming. A significant association between CTGF and HIF-1α levels was confirmed in placenta tissues and HTR8 cells under hypoxia. Our results suggest that an immune imbalance in the placenta causes FGR without other complications. We provide the first evidence for roles of CTGF in FGR and show that CTGF may function via HIF-1α-related pathways. Our findings elucidate the pathogenesis of FGR and provide new therapeutic targets.

Lower circulating preptin levels in male patients with osteoporosis are correlated with bone mineral density and bone formation.

BACKGROUND: Serum preptin levels among subjects with different bone mineral densities (BMD) were measured and investigated to determine the correlation between BMD and bone-metabolic markers. METHODS: Approximately 52 elderly male patients with osteoporosis, 50 elderly men with osteopaenia, and 31 age-matched normal bone mass controls participated in the study. The serum preptin levels and bone metabolic markers were measured by enzyme-linked immunosorbent assay. The relationships between preptin levels, BMD, and metabolic parameters were also assessed. RESULTS: The serum preptin level was the lowest in the osteoporosis group and positively correlated with BMD. All the bone formation markers in the osteoporosis and osteopaenia groups were significantly reduced compared with those in the normal group. Serum preptin level was positively correlated with all the bone formation markers, whereas no correlation was observed with the bone resorption marker TRACP-5b. CONCLUSIONS: Serum preptin levels are decreased in osteoporosis and osteopaenia patients and positively correlated with BMD. Therefore, preptin is involved in the pathogenesis of osteoporosis, probably through bone formation rather than bone resorption.