[The application of nanotopography in the development of tissue engineered tissues using mesenchymal stem cells].

Tissue engineering has emerged as a promising approach for the repair and functional reconstruction of damaged tissues. The bionic and intelligentized scaffolds provide the structural support for cell growth and differentiation as well as tissue regeneration. The surface properties of the biological material implant, the nanotopology in particular, become key aspects in determining the success of the implant. Mesenchymal stem cells (MSC) are widely favored by researchers as the seed cells in tissue engineering. Recently, it has been shown that nanotopographical characteristics of biomaterials regulate a wide range of MSC properties from their cellular behavior and differentiation potential. Herein, this review will provide an update on studies investigating the roles of nanotopography in the development of tissue engineering using MSC.

Case report: A case of hyperthyroidism secondary to bone metastasis of differentiated thyroid cancer.

It is usually believed that differentiated thyroid cancer is less likely to have distant metastases and rarely occurs secondary to hyperthyroidism. In our case report, we describe a patient diagnosed with thyroid fetal adenoma in 2002 who subsequently presented with a painful lump in her right rib. Through puncture biopsy, the mass was considered as metastatic follicular thyroid carcinoma, and then she appeared to have hyperthyroidism. The results of SPECT examination and other tests suggested that the hyperthyroidism was secondary to the thyroid cancer. The patient further underwent total thyroidectomy, and the pathology did not find any follicular thyroid foci. In this article, we analyze and discuss this case and review the relevant literature.

Causal associations between fluid intake patterns and dermatitis risk: a Mendelian randomization study.

Background: Dermatitis is one of the most common skin disorders across the world. Atopic dermatitis (AD) and contact dermatitis (CD) are its two primary types. Few studies have focused on the causal relationship between fluid intake and dermatitis. With an Mendelian Randomization (MR), this study investigated the potential causal effects of alcohol, coffee, tea, and water intake on the risk of AD and CD. Methods: Utilizing genetic variants as instrumental variables (IVs), a two-sample MR analysis was implemented based on data from the UK Biobank and FinnGen r9 consortium. Fluid intake was categorized into alcohol, coffee, tea, and water intake. Causal estimates were analyzed through Inverse Variance Weighted (IVW), MR-Egger, and weighted median methods. Cochran's Q, MR-Egger intercept, and MR-PRESSO tests were conducted to assess potential heterogeneity and pleiotropy. Results: Water intake exhibited a significant causal effect on raised CD risk (IVW OR = 2.92, 95% CI: 1.58-5.41, p = <0.01). Coffee intake was associated with increased CD risk (IVW OR = 2.16, 95% CI: 1.19-3.91, p = 0.01). Conversely, tea intake demonstrated a protective effect on AD risk (IVW OR = 0.71, 95% CI: 0.56-0.91, p = <0.01). Conclusion: This MR study suggests a potential association where water and coffee intake may be linked to an elevated risk of CD, while tea intake may potentially have a mitigating effect on AD risk. Modifying fluid intake patterns could be a targeted approach for dermatitis prevention, emphasizing the need for additional longitudinal studies to validate and expand upon these findings.

Data report on career adaptability, personal value, and motivational interview among at-risk Chinese college students.

The dataset provided here was partially associated with a published article on career adaptability [1]. The data set included 343 college freshmen who had difficulties in career decision-making. A self-report questionnaire on career adaptability (concern, control, curiosity, confidence), personal values (materialistic values, self-transcendence values, self-enhancement values), and demographic information was administered to all participants. In addition, a pre-selection of low career adaptability was performed. These participants scored below the 27th percentile in career adaptability. The career adaptability was administrated again two months later. We divided the data into two groups (intervention and control) and two time points (pre-test and post-test). Researchers can use the data to explore the relationship among career adaptability, personal values, and demographic information, as well as to compare interventions on career adaptability.

Body Dissatisfaction and Restricted Diet in Chinese Adolescents: A Longitudinal Analysis.

Background/Objective: Body dissatisfaction and restricted diet frequently co-occur among adolescents. However, the exact temporal relationship between the two is unclear. Furthermore, most relevant studies concentrate on Western cultural backgrounds, with only a few investigations conducted in many non-Western developing countries, including China. Therefore, this study aimed to investigate the mutual relationship between body dissatisfaction and restricted diet among Chinese adolescents. Patients/Methods: We recruited a sample of 672 middle school students from China (358 females, mean age = 14.33±0.94) and collected self-reported measures of body dissatisfaction and restricted diet at three-time points (with a five-month interval between each). We used cross-lagged models to examine the bidirectional relationship between body dissatisfaction and restricted diet. Results: (1) Both cross-sectional and cross-lagged correlation analysis showed positive correlation between body dissatisfaction and restricted diet (r=0.29-0.36; r=0.25-0.35, Ps<0.001); (2) The cross-lagged effect of body dissatisfaction on restricted diet was significant (ß=0.09, 0.13, Ps<0.01), and vice versa (ß=0.20, 0.18, Ps<0.001); (3) The differences in the associations between body dissatisfaction and restricted diet across gender were found. Conclusion/Implications: There is a bidirectional relationship between adolescents' body dissatisfaction and restricted diet. Our findings enrich the existing literature on body image and dietary health, thereby contributing to the reduction of negative body image and disordered eating among adolescents.

Targeting Super-Enhancer-Driven Oncogenic Transcription by CDK7 Inhibition in Anaplastic Thyroid Carcinoma.

Background: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancies, with no effective treatment currently available. The molecular mechanisms of ATC carcinogenesis remain poorly understood. The objective of this study was to investigate the mechanisms and functions of super-enhancer (SE)-driven oncogenic transcriptional addiction in the progression of ATC and identify new drug targets for ATC treatments. Methods: High-throughput chemical screening was performed to identify new drugs inhibiting ATC cell growth. Cell viability assay, colony formation analysis, cell-cycle analysis, and animal study were used to examine the effects of drug treatments on ATC progression. Chromatin immunoprecipitation sequencing was conducted to establish a SE landscape of ATC. Integrative analysis of RNA sequencing, chromatin immunoprecipitation sequencing, and CRISPR/Cas9-mediated gene editing was used to identify THZ1 target genes. Drug combination analysis was performed to assess drug synergy. Patient samples were analyzed to evaluate candidate biomarkers of prognosis in ATC. Results: THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), was identified as a potent anti-ATC compound by high-throughput chemical screening. ATC cells, but not papillary thyroid carcinoma cells, are exceptionally sensitive to CDK7 inhibition. An integrative analysis of both gene expression profiles and SE features revealed that the SE-mediated oncogenic transcriptional amplification mediates the vulnerability of ATC cells to THZ1 treatment. Combining this integrative analysis with functional assays led to the discovery of a number of novel cancer genes of ATC, including PPP1R15A, SMG9, and KLF2. Inhibition of PPP1R15A with Guanabenz or Sephin1 greatly suppresses ATC growth. Significantly, the expression level of PPP1R15A is correlated with CDK7 expression in ATC tissue samples. Elevated expression of PPP1R15A and CDK7 are both associated with poor clinical prognosis in ATC patients. Importantly, CDK7 or PPP1R15A inhibition sensitizes ATC cells to conventional chemotherapy. Conclusions: Taken together, these findings demonstrate transcriptional addiction in ATC pathobiology and identify CDK7 and PPP1R15A as potential biomarkers and therapeutic targets for ATC.

Sorafenib exerts an anti-keloid activity by antagonizing TGF-ß/Smad and MAPK/ERK signaling pathways.

Keloid disease is characterized by hyperproliferation of responsive fibroblasts with vigorously continuous synthesis of extracellular matrix (ECM) components. Although the process by which keloids develop is poorly understood, most theories of the etiology are referred to fibroblast dysfunction. A central event in dermal repair is the release of growth factors in response to skin injury, which leads to the dysregulation of several crucial pathways that initiate the activation of keloid fibroblasts (KFs) and promote ECM accumulation. Hence, strategies aimed at reducing the production of these cytokines and/or disrupting their intracellular signal transduction have potential clinical significance for curing keloid. As the first oral multikinase inhibitor, sorafenib blocks a number of intracellular signaling pathways which are also pivotal for keloid pathogenesis. Therefore, evaluation of the effects of sorafenib on keloid disease seems timely and pertinent. In this study, we reported the identification of sorafenib that antagonized TGF-ß/Smad and MAPK/ERK signaling pathways in primary KFs. Impressively, treatment with sorafenib inhibited KF cell proliferation, migration, and invasion, and simultaneously reduced collagen production in KFs. Furthermore, we present ex vivo evidence that sorafenib induced the arrest of KF migration, the inhibition of angiogenesis, and the reduction of collagen accumulation. These preclinical observations suggest that sorafenib deserves systematic exploration as a candidate agent for the future treatment of keloids. KEY MESSAGE: The intracellular TGF-ß/Smad and MAPK/ERK signaling pathways is blocked by sorafenib. Sorafenib inhibits the proliferation, migration, invasion, and ECM deposition in keloid fibroblasts. Sorafenib reduces KF migration and concomitantly angiogenesis in keloid explants. Sorafenib is a promising agent for the treatment of keloids and hypertrophic scars.