Study on the Effectiveness of Newman's System Model of Care in the Perioperative Period of Endometrial Cancer Patients.

Objective: The purpose of this study was to investigate the effectiveness of the Newman System model of care in the perioperative period for patients with endometrial cancer, to investigate the impact on psychological well-being, quality of life, and patient satisfaction. Methods: One hundred and eight patients with endometrial cancer who were treated in our hospital from January 2020 to January 2023 were selected as research subjects and were randomly divided into the control group (n=54) and the research group (n=54); the control group received conventional nursing care, and the research group added nursing care based on the conventional nursing care with Newman's systematic nursing care model including primary, secondary and tertiary care, comparing the psychological state score, quality of life score, coping style score, and satisfaction with nursing care of the two groups. Results: After the intervention, the anxiety self-assessment scale (SAS) and depression self-assessment scale (SDS) scores decreased in both groups, with the research group having lower scores than the control group (P < .05). After the intervention, all Oncology Quality of Life Core Questionnaire (QLQ-C30) scores increased in both groups, with the research group having higher scores than the control group (P < .05). After the intervention, avoidance and submission scores decreased in both groups, with the research group having lower scores than the control group (P < .05); coping scores increased in both groups, with the research group having higher scores than the control group (P < .05). Satisfaction with care was higher in the research group than in the control group (P < .05). Conclusion: The Newman's system model of care is effective in the perioperative period of endometrial cancer, helping to reduce patients' negative emotions, optimize coping, improve quality of life and nursing satisfaction, and has great value in clinical application and promotion.

Identification of a novel transthyretin mutation D39Y in a cardiac amyloidosis patient and its biochemical characterizations.

Hereditary transthyretin cardiac amyloidosis (hATTR-CA) is a rare autosomal dominantly inherited disease caused by mutations in the transthyretin (TTR) gene. TTR mutations often cause the instability of transthyretin, production of misfolded proteins, and ultimately excessive deposition of insoluble amyloid fibrils in the myocardium, thereby leading to cardiac dysfunction. Herein, we report a novel transthyretin D39Y mutation in a Chinese family. We characterized the kinetic and thermodynamic stabilities of D39Y mutant TTR, revealing that TTR D39Y mutant was less stable than WT TTR and more stable than amyloidogenic mutation TTR L55P. Meanwhile, the only FDA approved drug Tafamidis showed satisfactory inhibitory effect toward ATTR amyloid formation and strong binding affinity in test tube revealed by isothermal titration calorimetry. Finally, we measured the well-folded tetrameric TTR concentration in patient's and his descents' blood serum using a previously reported UPLC-based assay. Notably, the tetramer concentrations gradually increased from symptomatic D39Y gene carrier father, to asymptomatic D39Y gene carrier daughter, and further to wild type daughter, suggesting the decrease in functional tetrameric TTR concentration may serve as an indicator for disease age of onset in D39Y gene carriers. The study described a Chinese family with hATTR-CA due to the TTR variant D39Y with its destabilizing effect in both kinetic and thermodynamic stabilities.

Considering Psychosocial Factors When Investigating Blood Pressure in Patients with Short Sleep Duration: A Propensity Score Matched Analysis.

Few studies have considered psychosocial characteristics when investigating the associations between sleep duration and blood pressure (BP). In this study, we took propensity score matching (PSM) to adjust for psychosocial characteristics when comparing BP between individuals with short sleep duration and those with normal sleep duration. A total of 429 participants were included. 72 participants with sleep duration ≤6 h and 65 participants with sleep duration >6 h were matched after PSM. We compared office BP, 24-hour BP, and prevalence of hypertension in the populations before and after PSM, respectively. In the unmatched population, participants with sleep duration ≤6 h were observed with higher office diastolic BP (DBP) and 24-h systolic BP (SBP)/DBP (all P < 0.05). In the matched populations, the differences between the two groups (sleep duration ≤6 h vs. sleep duration >6 h) in office DBP (88.4 ± 10.9 vs. 82.5 ± 11.1 mm Hg; P=0.002), 24-h SBP (134.7 ± 12.0 vs. 129.3 ± 11.6 mm Hg; P=0.009), and 24-h DBP (83.4 ± 9.9 vs. 78.1 ± 10.1 mm Hg; P=0.002) become more significant. Participants with sleep duration ≤6 h only show higher prevalence of hypertension based on 24-h BP data, while analysis after PSM further revealed that these with sleep duration ≤6 h presented about 20% higher prevalence of elevated BP up to office diagnosed hypertension threshold. Therefore, psychosocial characteristics accompanied with short sleep duration should be fully valued in individuals at risks for elevated BP. This trial is registered with NCT03866226.

TBX20 Contributes to Balancing the Differentiation of Perivascular Adipose-Derived Stem Cells to Vascular Lineages and Neointimal Hyperplasia.

BACKGROUND: Perivascular adipose-derived stem cells (PVASCs) can contribute to vascular remodeling, which are also capable of differentiating into multiple cell lineages. The present study aims to investigate the mechanism of PVASC differentiation toward smooth muscle cells (SMCs) and endothelial cells (ECs) as well as its function in neointimal hyperplasia. METHODS: Single-cell sequencing and bulk mRNA sequencing were applied for searching key genes in PVASC regarding its role in vascular remodeling. PVASCs were induced to differentiate toward SMCs and ECs in vitro, which was quantitatively evaluated using immunofluorescence, quantitative real-time PCR (QPCR), and Western blot. Lentivirus transfections were performed in PVASCs to knock down or overexpress TBX20. In vivo, PVASCs transfected with lentivirus were transplanted around the guidewire injured femoral artery. Hematoxylin-eosin (H&E) staining was performed to examine their effects on neointimal hyperplasia. RESULTS: Bulk mRNA sequencing and single-cell sequencing revealed a unique expression of TBX20 in PVASCs. TBX20 expression markedly decreased during smooth muscle differentiation while it increased during endothelial differentiation of PVASCs. TBX20 knockdown resulted in the upregulation of SMC-specific marker expression and activated Smad2/3 signaling, while inhibiting endothelial differentiation. In contrast, TBX20 overexpression repressed the differentiation of PVASCs toward smooth muscle cells but promoted endothelial differentiation in vitro. Transplantation of PVASCs transfected with TBX20 overexpression lentivirus inhibited neointimal hyperplasia in a murine femoral artery guidewire injury model. On the contrary, neointimal hyperplasia significantly increased in the TBX20 knockdown group. CONCLUSION: A subpopulation of PVASCs uniquely expressed TBX20. TBX20 could regulate SMC and EC differentiation of PVASCs in vitro. Transplantation of PVASCs after vascular injury suggested that PVASCs participated in neointimal hyperplasia via TBX20.

Cardiac Adipose Tissue Contributes to Cardiac Repair: a Review.

Cardiac adipose tissue is a metabolically active adipose tissue in close proximity to heart. Recent studies emphasized the benefits of cardiac adipose tissue in heart remodeling, such as reducing infarction size, enhancing neovascularization and regulating immune response, through a series of cellular mechanisms. In the present manuscript, we provide a comprehensive review regarding the role of cardiac adipose tissue in cardiac repair. We focus on different cardiac adipose tissues according to their distinguished anatomical structures. This review summarizes the latest evidence on the relationship between cardiac adipose tissue and cardiac repair. Cardiac adipose tissues (CAT) were systematically reviewed in the current manuscript which focused on the components of CAT, debates about cardiac adipose stem cells and their effect on heart.

Prognostic significance of left anterior fascicular block and its relation with coronary artery disease in old patients based on 570 autopsy cases.

BACKGROUND: Left Anterior Fascicular Block (LAFB) occurs frequently among the elderly, and have a correlation with coronary artery disease (CAD), yet controversies regarding its clinical significance still remain. METHODS: We carried on a retrospective study involving 92 LAFB and 478 non-LAFB patients, in which anatomic, clinical and electrocardiographic characteristics were compared. RESULTS: LAFB subjects had more pathological CAD (66.3% vs 54.6%, P = 0.039), myocardial infarction (MI) (53.3% vs 37.9%, P = 0.007) and myocarditis (5.4% vs 1.7%, P = 0.043). Among the LAFB group, 58.1% of patients with CAD and 30.2% of patients with MI were clinically misdiagnosed, while 42.9% of patients with MI were clinically missed. Logistic regression showed CAD had no independent relevance with LAFB. LAFB subjects displayed heavier hearts [(451.1 ±â€¯101.3)g vs (407.1 ±â€¯102.3)g, P < 0.001], thicker left ventricular walls [(1.6 ±â€¯0.4)cm vs (1.4 ±â€¯0.3)cm, P = 0.001]. Kaplan-Meier survival analysis indicated significant differences in long-term survival time (χ2 = 12.223, P < 0.001) and cardiac mortality (χ2 = 20.982, P < 0.001) between LAFB and non-LAFB group. Cox multivariate analysis demonstrated LAFB was an independent risk factor of all-cause death (HR = 1.552, 95% CI = 1.208-1.994, P = 0.001) and cardiac death (HR = 2.287, 95% CI = 1.545-3.386, P < 0.001). The major death cause of LAFB was cardiac death (46.7%), including more MI (28.3% vs 13.4%, P = 0.008), myocarditis (4.3% vs 1.0%, P = 0.042) and cardiac rupture (6.7% vs 1.9%, P = 0.022). CONCLUSIONS: LAFB subjects had more pathological CAD and MI, but LAFB was not an independent relevant factor of CAD. LAFB lowered the accuracy to clinically diagnose CAD. LAFB patients gained heavier hearts, thicker left ventricular walls, and suffered increased risk of death and cardiac death.