Is Type 2 Diabetes Mellitus Associated with Spinal Degenerative Disorders?: Evidence from Observational and 2-Sample Mendelian Randomization Analyses.

BACKGROUND: Type 2 diabetes mellitus (T2DM) and spinal degenerative disorders (SDD) are common diseases that frequently coexist. However, both traditional observational studies and recent Mendelian randomization (MR) studies have demonstrated conflicting evidence on the association between T2DM and SDD. This comparative study explored and compared the association between T2DM and SDD using observational and MR analyses. METHODS: For observational analyses, cross-sectional studies (44,972 participants with T2DM and 403,095 participants without T2DM), case-control studies (38,234 participants with SDD and 409,833 participants without SDD), and prospective studies (35,550 participants with T2DM and 392,046 participants without T2DM with follow-up information until 2022) were performed to test the relationship between T2DM and SDD using individual-level data from the U.K. Biobank from 2006 to 2022. For MR analyses, the associations between single-nucleotide polymorphisms with SDD susceptibility obtained using participant data from the U.K. Biobank, which had 407,938 participants from 2006 to 2022, and the FinnGen Consortium, which had 227,388 participants from 2017 to 2022, and genetic predisposition to T2DM obtained using summary statistics from a pooled genome-wide association study involving 1,407,282 individuals were examined. The onset and severity of T2DM are not available in the databases being used. RESULTS: Participants with T2DM were more likely to have SDD than their counterparts. Logistic regression analysis identified T2DM as an independent risk factor for SDD, which was confirmed by the Cox proportional hazard model results. However, using single-nucleotide polymorphisms as instruments, the MR analyses demonstrated no causal relationship between T2DM and SDD. The lack of such an association was robust in the sensitivity analysis, and no pleiotropy was seen. CONCLUSIONS: Our results suggest that the association between T2DM and SDD may be method-dependent. Researchers and clinicians should be cautious in interpreting the association, especially the causal association, between T2DM and SDD. Our findings provide fresh insights into the association between T2DM and SDD by various analysis methods and guide future research and clinical efforts in the effective prevention and management of T2DM and SDD. LEVEL OF EVIDENCE: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

The relationship between psychological distress and cognitive failure among breast cancer survivors: a network analysis.

Background: Psychological distress is highly prevalent and has a severe impact on the quality of life among breast cancer survivors. This type of distress is associated with cognitive failure. However, previous studies have focused solely on the total scale scores of these two concepts while ignoring the unique relationship between specific components. In the present study, we utilized network analysis to explore the relationship between psychological distress and cognitive failure in breast cancer survivors. Methods: The network analysis approach was adopted to estimate the regularized partial correlation network in a cross-sectional sample of 409 breast cancer survivors. All participants were assessed using the Depression Anxiety Stress Scale and the Cognitive Failure Questionnaire. The Gaussian Graphical Model was employed to estimate the network, centrality indices, and edge weights, providing a description of the characteristics of the network. Results: The results indicated that anxiety-stress and depression-stress were the strongest edges in the community of psychological distress. Distractibility-memory was the strongest edge in the community of cognitive failure. Distractibility and memory were the most central nodes, with the highest expected influence in the network. Depression and motor coordination acted as important bridge nodes with the highest bridge expected influence. Conclusion: Distractibility and memory in cognitive failure played important roles in activating and maintaining the relationship network. Motor coordination was identified as the crucial pathway for the impact of cognitive failure on psychological distress. Interventions targeting these specific issues might be more effective in improving cognitive failure and reducing psychological distress among breast cancer survivors.

Impact of Gender-Role Attitudes and Mental Health on Hostile Sexism and Acceptance of Cosmetic Surgery.

BACKGROUND: Each year, tens of thousands of people worldwide choose to undergo cosmetic surgery in order to alter their appearance. In recent years, young people have gradually emerged to comprise the main driving force behind the increasing demand for cosmetic surgery. Previous studies have found that sexism may motivate young people to undergo such surgeries. However, few studies have been conducted to determine if this psychological mechanism influences the acceptance of cosmetic surgery among Chinese university students. METHODS: A total of 579 Chinese university students (280 girls and 299 boys, 17-20 years) volunteered to participate in the online survey. They completed a questionnaire containing the Ambivalent Sexism Inventory, the 12-item General Health Questionnaire, the Gender-Role Attitudes Questionnaire and the Acceptance of Cosmetic Surgery Scale. We firstly evaluated the underlying factor structure of the Acceptance of Cosmetic Surgery Scale using exploratory and confirmatory factor analyses, and exploring pattern of associations between the constructs was analyzed via path analysis. RESULTS: According to the findings, hostile sexism was associated with greater levels of acceptance toward cosmetic surgery. Moreover, gender-role attitudes mediated the link between hostile sexism and the acceptance of cosmetic surgery, and this mediation was positively influenced by general mental health. CONCLUSION: Our study contributes to a deeper understanding of Chinese university students' attitudes toward cosmetic surgery, hostile sexism may contribute to normalizing traditional gender stereotypes and encourage cosmetic surgery acceptability among Chinese university students. LEVEL OF EVIDENCE V: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Spinal infection after vertebral augmentation: a covert complication with serious havoc.

INTRODUCTION: Vertebral augmentation, including percutaneous vertebroplasty (PVP) or kyphoplasty (PKP), is the current least invasive surgical option and has been widely used to treat the painful osteoporotic vertebral compression fractures (OVCF). However, the postoperative infections could be life-threatening, even though they rarely occur. Our studies aim to clarify the causation and outcomes of spinal infections following augmentation and meanwhile to identify the risk factors. METHODS: A retrospective study was conducted on patients with OVCF who underwent PVP or PKP, and were subsequently admitted to our institution with postoperative spinal infection between January 2010 and December 2022. A total of 33 patients were finally included. RESULTS: The rate of spinal infection after augmentation in our single institute was 0.05% (2/3893). In addition to these 2 patients, the remaining 31 were referred from other hospitals. All 33 patients exhibited elevated inflammatory parameters, 14 patients presented with fever, and 9 patients experienced neurological deficits. Additionally, 29 patients had comorbidity and risk factors. Pathogens were identified in 26 patients, while only 7 patients were examined as culture negative. 27 patients underwent revision surgery and 6 patients only received conservative therapy. Anterior surgery was performed in 2 patients, while posterior surgery was performed in 20 patients. A combined anterior-posterior surgery was performed in 5 patients. At the final follow-up, 18 patients had unrestricted mobility, 10 patients required assistance from crutches or a walker for ambulation, 4 patients needed a wheelchair, and 1 patients died after revision surgery. CONCLUSIONS: Spinal infection after vertebral augmentation is rare, but it cannot be ignored. Surgeons should make every effort to detect the potential preoperative spondylitis or discitis. Once postoperative spinal infection is confirmed, a prompt intravenous antibiotic therapy is warranted. If medication therapy fails, revision surgery involving debridement and spinal reconstruction should be considered.

Thrombospondin-1 mimic peptide PKHB1 induced endoplasmic reticulum stress-mediated but CD47-independent apoptosis in non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is one of the most common malignancies with high morbidity and mortality. PKHB1, a serum-stable Thrombospondin-1 (TSP-1) mimic peptide, has shown some effective ability in triggering cell death against several cancers. Here, we aimed to study the potential biological function of PKHB1 and its molecular mechanism in NSCLC. Our results revealed that PKHB1 significantly suppressed NSCLC cell proliferation, cell migration, and induced apoptosis in a dose-dependent manner. Additionally, we found that PKHB1 treatment resulted in mitochondrial transmembrane potential depolarization, Ca2+ overloading as well as the upregulation of proapoptotic proteins. Mechanistically, PKHB1 induced NSCLC cells apoptosis in a CD47-independent manner. Further study revealed that PKHB1 provoked endoplasmic reticulum (ER) stress principally through the activation of CHOP and JNK signaling, which could be alleviated in the presence of 4-PBA, an ER stress inhibitor. Furthermore, xenograft tumor models showed that PKHB1 treatment could notably inhibit NSCLC tumor growth in vivo. In conclusion, these findings suggested that PKHB1 exerted antitumor efficacy in NSCLC via triggering ER stress-mediated but CD47-independent apoptosis, potentially functioned as a promising peptide-based therapeutic agent for NSCLC.

Is 3D-printed prosthesis stable and economic enough for anterior spinal column reconstruction after spinal tumor resection? A retrospective comparative study between 3D-printed off-the-shelf prosthesis and titanium mesh cage.

OBJECT: To investigate the stability and cost-effectiveness of the three-dimensional-printed (3DP) off-the-shelf (OTS) prosthesis in the reconstruction of the anterior column of the thoracic/lumbar spine after tumor resection. METHODS: Thirty-five patients (26 with primary malignant tumors and nine with metastatic malignant tumors) who underwent tumor resection and anterior column reconstruction between January 2014 and January 2019 were included in a single institute. Patients were divided into the 3DP OTS prosthesis (3DP) group (n = 14) and the titanium mesh cage (TMC) group (n = 21) by the type of implant. The operation time, intraoperative blood loss, hospital stay, history of radiotherapy, surgical level and total cost were collected and compared between the two groups. Mechanical complications and radiological parameters including mean vertebral height, subsidence, fixation failure(nonunion, migration, screw loosening, rod breakage) rate were recorded at preoperation, 1 week, 3 months, 6 months, 12 months after surgery then at 1 year interval or stop until the end of survival. The follow-up patients were also sent with short form-36 to assess their health-related quality of life (HRQoL) and questions about the current condition of their disease. RESULTS: The mean overall follow-up was 24.6 months. Of the 35 patients involved, six patients died and six were lost to follow-up. The differences between the two groups in operative time, intraoperative blood loss, and hospital stay were not statistically significant (p > 0.05). The differences in fixation failure and the subsidence rate between the two groups were not statistical significant (p > 0.05). The difference of subsidence rate between the cases with and without osteoporosis, cases with and without radiotherapy was statistically significant within each group (p < 0.05). However, the difference of subsidence rate between the surgical level above or below T10 was not statistically significant (p > 0.05). The response rate of the questionnaire among the survived patients was 100% (23/23 patients). The results of the Short Form- (SF-)36 between the two groups were similar (p > 0.05). The total cost was higher in the 3DP group (p < 0.05) with its higher graft cost (p < 0.05), but the differences in internal fixation cost and other cost were not statistically significant between groups (p > 0.05). CONCLUSION: Compared to TMC, the 3DP OTS prosthesis achieved similar clinical and radiological results in spinal anterior spinal column reconstruction of thoracic/lumbar spinal tumor resection. However, the 3DP OTS prosthesis was more expansive than TMC.

Application of MRI and CT Images in Surgical Treatment of Early Cervical Cancer.

In order to understand the problems of the application of MRI and CT images in the early cervical cancer surgery, a method that the application of MRI imaging and CT images in early cervical cancer surgery was proposed. For the cervical cancer in clinical practice, the applications of the modern imaging examination and the clinical staging classification were investigated and analyzed. Compared with the surgical pathology results, the application value of common modern imaging in clinical staging of cervical cancer was evaluated. It was found that the sensitivity of MRI and CT in diagnosing lymph node metastasis was 56% and 58%, and the specificity was 93% and 92%, respectively. The experiment proved the application value of MRI and CT in clinical staging of cervical cancer.

Th22 Cells/IL-22 Serves as a Protumor Regulator to Drive Poor Prognosis through the JAK-STAT3/MAPK/AKT Signaling Pathway in Non-Small-Cell Lung Cancer.

The interaction of immune cells and cytokines in the tumor microenvironment affects the development and prognosis of tumors with an unclear potential regulatory mechanism. Recent studies have elucidated the protumor role of Th22 cells and its lineage-specific cytokine IL-22 in different human cancers. The present study is aimed at investigating the biological effect of Th22 cells/IL-22 and its molecular mechanism in the pathogenesis process of non-small-cell lung cancer (NSCLC). It was initially found that Th22 cells were enriched in the peripheral blood of NSCLC patients. The level of Th22 cells in peripheral blood mononuclear cells (PBMCs) was positively correlated with the TNM stage, lymph node metastasis, and clinical tumor biomarkers. Furthermore, IL-22 not only antagonized the apoptosis inducing and cell cycle arresting effect by chemotherapy and molecular targeted drugs on NSCLC cell lines but also promoted tumor cell proliferation and tumor tissue growth. Moreover, IL-22 activated the JAK-STAT3/MAPK/AKT signaling pathway, both in vitro and in vivo. Conclusively, the present results confirm that Th22 cells/IL-22 may serve as a negative immune regulator in lung cancer.

Deguelin Attenuates Non-Small-Cell Lung Cancer Cell Metastasis by Upregulating PTEN/KLF4/EMT Signaling Pathway.

Non-small-cell lung cancer (NSCLC) is the most common lung cancer and a major cause of cancer mortality worldwide. Deguelin plays a vital inhibitory role in NSCLC initiation and development. However, the downstream mechanism of deguelin-suppressed metastasis of NSCLC cells is still not completely understood. Interestingly, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and Krüppel-like factor 4 (KLF4) also contribute to inhibition of metastasis in NSCLC cells. Here, we demonstrated that deguelin significantly upregulated PTEN and KLF4 expressions and PTEN positively upregulated KLF4 expression in NSCLC cells including A549 and PC9 cells. Moreover, overexpressions of PTEN and KLF4 inhibited the migration and invasion of NSCLC cells, an effect similar to that of deguelin. Furthermore, overexpressions of PTEN and KLF4 could suppress the epithelial-mesenchymal transition (EMT), an effect also similar to that of deguelin. Additionally, deguelin displayed a significant antitumor ability by upregulating PTEN and KLF4 expressions in mice model with NSCLC cells. Together, these results indicated that deguelin could be a potential therapeutic agent through upregulating PTEN and KLF4 expressions for NSCLC therapy.

IL-17A contributes to skeletal muscle atrophy in lung cancer-induced cachexia via JAK2/STAT3 pathway.

Cachexia is a complex metabolic syndrome that occurs in approximately 50% of patients with cancer. Skeletal muscle atrophy is the primary clinical feature. Interleukin (IL)-17A, a proinflammatory factor, plays an important role in many chronic inflammatory diseases. Here, we describe a novel signaling pathway through which IL-17A induced muscle atrophy. We conducted a retrospective clinical study to investigate the relationship between IL-17A and the skeletal muscle index in patients with lung adenocarcinoma. We also investigated the involvement of JAK2/STAT3 signaling pathway regarding the main features of cachexia by injecting Lewis lung carcinoma (LLC) cells into C57BL/6 mice as a model to replicate cancer-induced cachexia. In vitro, C2C12 myotubes were treated with recombinant IL-17A, anti-IL-17A monoclonal antibody, STAT3 inhibitor AG490, and LLC-conditioned medium. Cell viability and aging were also evaluated. We found that in cancer conditions, increased serum levels of IL-17A were related to muscle wasting. JAK2/STAT3 phosphorylation was observed in the muscle of LLC tumor-bearing mice, accompanied by decreased MHC/Myog levels and increased MuRF1/Atrogin-1 levels. Administration of anti-IL-17A monoclonal antibody and AG490 slowed muscle atrophy development. Consistent with the in vivo findings, C2C12 myotubes treated with IL-17A and LLC-conditioned medium demonstrated phosphorylated JAK2/STAT3 signaling, resulting in MHC loss and myotube atrophy. IL-17A also inhibited C2C12 cell proliferation, cell cycle breaking, and cellular senescence. Our results identify that phosphorylation of IL-17A/JAK2/STAT3 signaling pathway appears to be an important component in the pathogenesis of LLC tumor-induced cachexia. Targeted therapy of IL-17A may be a promising approach to reduce skeletal muscle loss in patients with cancer.

The relationship between post-traumatic stress and negative emotions in patients with breast cancer: the mediating role of emotion regulation.

Purpose:Negative emotions can adversely affect the treatment and recovery of breast cancer patients. Post-traumatic stress caused by cancer can increase the negative emotions of patients. This study assessed the relationship between post-traumatic stress and emotional regulation strategies, and the role of emotional regulation in the relationship between post-traumatic stress and negative emotions in breast cancer patients.Design:Cross-sectional questionnaire with sample of 214 Chinese women with breast cancerMethods:Participants completed the Impact of Event Scale-Revised, Hospital Anxiety and Depression Scale, and Emotion Regulation Questionnaire. Correlation and mediation analyses were conducted to assess associations among the scores of these scales.Findings:Patients with low post-traumatic stress chose cognitive reappraisal strategies, while those with high post-traumatic stress chose expressive suppression strategies. Cognitive reappraisal had a significant negative predictive effect on negative emotions, while expressive suppression had a significant positive predictive effect on patient's negative emotions.Conclusions:Cognitive reappraisal may reduce the impact of post-traumatic stress on negative emotions experienced by breast cancer patients. Implications for psychosocial providers or policy: Psychosocial workers in China should conduct cognitive reappraisal training for breast cancer patients with high negative emotions and severe post-traumatic stress. For Chinese breast cancer patients living in other regions, the local oncology social workers should take into account their cultural background and lack of expression, and encourage them to choose cognitive reappraisal strategies.

A novel stilbene derivative (GMQ3) suppressed proliferation and induced apoptosis in lung cancer via the p38-MAPK/SIRT1 pathway.

BACKGROUND: Lung cancer is the primary cause of cancer-related mortality worldwide. The anticancer effect of stilbene has been noted in various tumor types. GMQ3, which has a stilbene-mimicking skeleton, is a novel small-molecule compound with promising antitumor activity. Our results revealed that GMQ3 not only suppressed cell proliferation and cell migration of lung cancer cells but also led to G1 phase cell cycle arrest and triggered caspase-dependent apoptosis. Furthermore, investigation of the molecular mechanism showed that GMQ3 could inhibited proliferation and induced apoptosis via the p38-MAPK/SIRT1 pathway both in vitro and in vivo. Xenograft tumor mouse models showed that GMQ3 significantly inhibited tumor growth in vivo without affecting body weight. Our findings indicated that GMQ3 exerts a strong anticancer action by suppressing cell proliferation, inhibiting cell migration and inducing cell apoptosis. Moreover, the efficacy of GMQ3 was enhanced in the presence of CDK4/6 inhibitor Abemaciclib. We conclude that GMQ3 is a promising agent with potential for lung cancer.

VIRMA contributes to non-small cell lung cancer progression via N6-methyladenosine-dependent DAPK3 post-transcriptional modification.

N6-methyladenosine (m6A) has been reported to be abnormally expressed in non-small cell lung cancer (NSCLC), and plays a vital role in regulation of cell proliferation, invasion and metastasis. Vir-Like m6A methyltransferase associated (VIRMA, also called KIAA1429) has not been well studied in NSCLC. Thus, in this study, we investigated the biological impact and underlying mechanism of VIRMA in NSCLC. High expression of VIRMA was testified in patients with NSCLC and predicted worse prognosis in patients. VIRMA facilitated cell proliferation and tumor growth both in vitro and in vivo. Furthermore, VIRMA-regulated m6A modifications led to post-transcriptional suppression of death-associated protein kinase 3 (DAPK3, also called ZIP or ZIPK) through the YT521-B homology domain-containing family proteins 2/3(YTHDF2/3). Inhibition of DAPK3 rescued the tumor-suppressive phenotypes induced by VIRMA deficiency. In conclusion, VIRMA-guided m6A modifications promoted NSCLC progression via m6A-dependent degradation of DAPK3 mRNA. Therefore, VIRMA may be a novel therapeutic target in NSCLC.

Eosinophils may serve as CEA-secreting cells for allergic bronchopulmonary aspergillosis (ABPA) patients.

Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterized by an exaggerated response of the immune system to the fungus Aspergillus. This study aimed to assess the relationship between carcinoembryonic antigen (CEA) and eosinophils in ABPA patients. We describes a case of a 50-year-old patient who was diagnosed with ABPA presenting with high level of CEA and eosinophils. Besides,we used immunohistochemistry and immunofluorescence to identify eosinophils and CEA in sections which were obtained by Endobronchial ultrasound-guided transbronchial lung biopsy aspiration (EBUS-TBLB). The sections were then visualized using confocal microscopy. We also retrospectively analyzed a cohort of 37 ABPA patients between January 2013 and December 2019 in our hospital. We found the patient whose serum CEA levels were consistent with eosinophils during the follow-up (r = 0.929, P = 0.022). The positive expression of CEA and abnormal expression of eosinophils was higher in the ABPA tissue compared to the normal lung tissue. The co-localization was represented as pixels containing both red and green color in the image (with various shades of orange and yellow) which signified that eosinophils were immunohistochemically positive for CEA. Patients with higher levels of eosinophils had higher levels of CEA in the serum (P < 0.001). The results of Pearson correlation analysis showed that the levels of eosinophils were positively correlated with serum CEA levels (r = 0.459 and r = 0.506, P = 0.004 and P = 0.001). Serum CEA level is elevated in ABPA patients. The elevated serum CEA level was shown to be normalized after treatment. Increased CEA levels in ABPA patients may be positively correlated with eosinophil levels, and eosinophils may be served as CEA-secreting cells in patients with ABPA.

Dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathways in lung squamous cell carcinoma.

Lung squamous cell carcinoma (SCC) is one of the deadliest cancers both in China and worldwide. To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin. In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC.

Full-Endoscopic Posterior Lumbar Interbody Fusion Via an Interlaminar Approach Versus Minimally Invasive Transforaminal Lumbar Interbody Fusion: A Preliminary Retrospective Study.

OBJECTIVES: Minimally invasive transforaminal lumbar interbody fusion (MIS-TLIF) has been performed as a minimally invasive surgery for lumbar degenerative disease, but previous MIS-TLIF methods have shown limitations by their own characters. In this study, we developed a newly interbody fusion technique of full-endoscopic posterior lumbar interbody fusion (FE-PLIF) via an interlaminar approach, presented its preliminary clinical results in comparison with MIS-TLIF procedure. METHODS: This study retrospectively reviewed 52 patients who underwent FE-PLIF (n = 22) or MIS-TLIF (n = 30) surgery between October 2018 and February 2019. Patient demographics, intraoperative parameters, and perioperative complications were collated. Clinical and radiologic outcomes were evaluated at each follow-up for up to 12 months. RESULTS: FE-PLIF demonstrated a longer operation time, less blood loss, and shorter hospitalization duration than MIS-TLIF. The visual analog scale (VAS) score for leg pain in both groups and for back pain in FE-PLIF group significantly improved at 1 week, while the VAS score for back pain in MIS-TLIF group significantly improved at 3 months. No significant difference in the VAS and Oswestry disability index scores was found between the groups at 3 months and 12 months. Fusion rates of definite grades were not significantly different between the groups (73.3% vs. 70.0%, P > 0.05). All patients who suffered from cage subsidence or nonunion were asymptomatic and did not require revision surgery during the follow-up. CONCLUSIONS: The FE-PLIF interlaminar approach is a safe and effective interbody fusion technique with less surgical trauma and similar outcomes compared to MIS-TLIF. However, this technique still requires technical advancements to improve efficiency and reduce technical complexity.

Difficulties in identifying and describing feelings, social constraints, affect, and functional well-being among Chinese breast cancer patients: A mediation model.

PURPOSE: Functional well-being (i.e., individuals' functioning in daily living activities and social roles; FWB) is often an understudied aspect of quality of life among breast cancer patients (BCP). Previous research has suggested that patients' emotional experience is associated with their FWB. However, little is known about how intrapersonal and interpersonal barriers of emotional processing and expression (i.e., social constraints, difficulties in identifying and expressing emotions) associated with FWB among Chinese BCP, plus how positive/negative affect might explain such associations. METHOD: Chinese BCP (N = 327) in Weifang, Shandong province, China completed a cross-sectional survey. The Functional Well-Being subscale from the Chinese version of the Functional Assessment of Cancer Therapy-Breast (FACT-B), the Social Constraints Scale, the Difficulty in Identifying Feelings (DIF; 7 items) and the Difficulty in Describing Feelings (DDF; 5 items) subscales from the Toronto Alexithymia Scale and the Positive Affect and Negative Affect Schedule were used as assessment scales. RESULTS: Path analyses results supported the proposed mediation model with satisfactory fit indices (χ2(5) = 5.12, p = .40, CFI = 1.00; IFI = 1.00; RMSEA = 0.01). Specifically, difficulty in describing emotions was associated with poorer functional well-being through increased negative affect (ß = -0.06, 95%CI = -0.10, -0.03); difficulty in identifying emotions was associated with poorer functional well-being through reduced positive affect (ß = -0.04, 95%CI = -0.09, -0.003). Social constraints were associated with poorer functional well-being through both increased negative affect and decreased positive affect (ß = -0.16, 95%CI = -0.22, -0.10). After considering the mediators, difficulties in describing emotions still contributed significantly to functional well-being (ß = -0.20, 95%CI = -0.31, -0.08). Our results indicated that positive/negative affect could mediate between barriers of emotional processing/expression and FWB. CONCLUSIONS: This study was unique in revealing how intrapersonal and interpersonal barriers of emotional processing and expression could be associated with Chinese BCPs' FWB through varied mechanisms. Practitioners should consider strategies to reduce those barriers through interventions.

Combined Transplantation With Human Mesenchymal Stem Cells Improves Retinal Rescue Effect of Human Fetal RPE Cells in Retinal Degeneration Mouse Model.

Purpose: We verified whether fetal RPE (fRPE) cells and mesenchymal stem cells (MSCs) cotransplantation can combine the features of these two cell types and alleviate retinal degeneration in a retinal degenerative disease mouse model. Methods: Tail vein injection of sodium iodate (NaIO3) was conducted to establish the retinal degenerative disease mouse model. MSCs and fRPE cells were transplanted either separately or combined in the subretinal space of retinal degenerative disease animals. ERG, optical coherence tomography, histologic, and immunofluorescence analyses were performed. Furthermore, the expression level of Crx, rhodopsin, Iba1, F4/80, Caspase 3, nerve growth factor, and brain-derived neurotrophic factor were assessed to investigate the mechanisms involved in cell transplantation effects. Results: Cotransplantation of fRPE and MSC cells promoted significant improvements in ERG results and in the survival rate of transplanted cells. In addition, MSC and fRPE cell cotransplantation resulted in an increase in the thickness of the total retina, as well as in the outer and inner nuclear layers. Combined transplantation also upregulated the expression level of Crx and rhodopsin and downregulated caspase 3 expression, highlighting its better photoreceptor rescue effect in relation to the single cell type transplantation. Finally, combined transplantation suppressed the expression of Iba1 and F4/80 factors while increasing the endogenous expression of nerve growth factor and brain-derived nerve growth factor neurotrophic factors. These data suggest that MSC and fRPE cell cotransplantation is able to suppress immunoreactions and promote neurotrophic factor excretion. Conclusions: Combined transplantation of MSCs and fRPE cells results in a better retinal rescue effect than single cell type transplantation in NaIO3-induced retinopathy.

Dioscin elicits anti-tumour immunity by inhibiting macrophage M2 polarization via JNK and STAT3 pathways in lung cancer.

Tumour-associated macrophage (TAM) is an important component in tumour microenvironment. Generally, TAM exhibits the function of M2-like macrophage, which was closely related to angiogenesis and tumour progression. Dioscin, a natural steroidal saponin, has shown its powerful anti-tumour activity recently. However, the mechanism of dioscin involved in immune regulation is still obscure. Here, we observed dioscin induced macrophage M2-to-M1 phenotype transition in vitro and inhibited IL-10 secretion. Meanwhile, the phagocytosis of macrophages was enhanced. In subcutaneous lung tumour models, dioscin inhibited the augmentation of M2 macrophage populations. Furthermore, dioscin down-regulated STAT3 and JNK signalling pathways in macrophages in vitro. In BMDMs, activating JNK and inhibiting STAT3 induce macrophages to M1 polarization while inhibiting JNK and activating STAT3 to M2 polarization. Additionally, condition mediums from dioscin-pre-treated macrophages inhibited the migration of 3LL cells and the tube-formation capacity of HUVECs. What's more, dioscin-mediated macrophage polarization inhibited the in vivo metastasis of 3LL cells. In conclusion, dioscin may act as a new anti-tumour agent by inhibiting TAMs via JNK and STAT3 pathways in lung cancer.