Optical enhancement mode 2 improves the detection rate of gastric neoplastic lesion in high-risk populations: A multicenter randomized controlled clinical study.

OBJECTIVES: Detection of early neoplastic lesions is crucial for improving the survival rates of patients with gastric cancer. Optical enhancement mode 2 is a new image-enhanced endoscopic technique that offers bright images and can improve the visibility of neoplastic lesions. This study aimed to compare the detection of neoplastic lesions with optical enhancement mode 2 and white-light imaging (WLI) in a high-risk population. METHODS: In this prospective multicenter randomized controlled trial, patients were randomly assigned to optical enhancement mode 2 or WLI groups. Detection of suspicious neoplastic lesions during the examinations was recorded, and pathological diagnoses served as the gold standard. RESULTS: A total of 1211 and 1219 individuals were included in the optical enhancement mode 2 and WLI groups, respectively. The detection rate of neoplastic lesions was significantly higher in the optical enhancement mode 2 group (5.1% vs. 1.9%; risk ratio, 2.656 [95% confidence interval, 1.630-4.330]; p < 0.001). The detection rate of neoplastic lesions with an atrophic gastritis background was significantly higher in the optical enhancement mode 2 group (8.6% vs. 2.6%, p < 0.001). The optical enhancement mode 2 group also had a higher detection rate among endoscopists with different experiences. CONCLUSIONS: Optical enhancement mode 2 was more effective than WLI for detecting neoplastic lesions in the stomach, and can serve as a new method for screening early gastric cancer in clinical practice. CLINICAL REGISTRY: United States National Library of Medicine (https://www. CLINICALTRIALS: gov), ID: NCT040720521.

Astaxanthin Ameliorates Skeletal Muscle Atrophy in Mice With Cancer Cachexia.

Astaxanthin (AST) is a natural marine carotenoid with a variety of biological activities. This study aimed to demonstrate the possible mechanisms by which AST improves skeletal muscle atrophy in cancer cachexia. In this study, the effects of different doses of AST (30 mg/kg b.w., 60 mg/kg b.w. and 120 mg/kg b.w.) on skeletal muscle functions were explored in mice with cancer cachexia. The results showed that AST (30, 60 and 120 mg/kg b.w.) could effectively protect cachexia mice from body weight and skeletal muscle loss. AST dose-dependently ameliorated the decrease in myofibres cross-sectional area and increased the expression of myosin heavy chain (MHC). AST treatment decreased both the serum and muscle level of IL-6 but not TNF-α in C26 tumor-bearing cachexia mice. Moreover, AST alleviated skeletal muscle atrophy by decreasing the expression of two muscle-specific E3 ligases MAFBx and MuRF-1. AST improved mitochondrial function by downregulating the levels of muscle Fis1, LC3B and Bax, upregulating the levels of muscle Mfn2 and Bcl-2. In conclusion, our study show that AST might be expected to be a nutritional supplement for cancer cachexia patients.

Acute spontaneous vortex vein occlusion: clinical features, multimodal imaging and natural course.

AIMS: To describe the clinical features, multimodal imaging, treatments and natural course of acute spontaneous vortex vein occlusion. METHODS: Clinical data were collected on nine patients with acute vortex vein occlusion. The symptoms and signs, multimodal imaging, treatments and follow-up results were summarised. RESULTS: Six patients (66.7%) were men and three (33.3%) were women. The mean age was 47.8±15.4 years. Patients were initially misdiagnosed as having choroidal tumour (66.7%), scleritis (22.2%) and peripheral exudative haemorrhagic chorioretinopathy (11.1%). The related clinical characteristics included choroidal pseudo-tumour (100%), anterior segment injection (88.9%), acute ocular pain (77.8%), transient blurred vision (66.7%) and subsequent scleral icterus (66.7%). Six patients (66.7%) experienced a definite Valsalva manoeuvre prior to the onset. In acute phase, ultrasonography showed a low-to-medium reflective lesion without inside blood flow signal (mean thickness, 2.7±0.6 mm). Swept-source optical coherence tomography angiography (SS-OCTA) demonstrated the dilated vortex veins and ampulla with suprachoroidal haemorrhage and exudation. Indocyanine green angiography (ICGA) demonstrated choroidal circulation abnormalities in the affected quadrant. MRI showed a well-defined mass with enhancement. The main treatment was medical observation (44.5%). The choroidal pseudo-tumour spontaneously resolved with a mean course of 4.1±1.9 weeks. CONCLUSIONS: Acute vortex vein occlusion is a rare condition and initial misdiagnosis is not uncommon. It is mainly identified as an evanescent choroidal pseudo-tumour with acute pain, red eye and blurred vision. Widefield ICGA and SS-OCTA can offer valuable diagnostic clues. Medical observation may be a treatment option.

Isorhamnetin ameliorates cisplatin-induced acute kidney injury in mice by activating SLPI-mediated anti-inflammatory effect in macrophage.

OBJECTIVE: Isorhamnetin (IH) has been reported to have significant anti-inflammatory effects in various diseases, but its role and mechanism in AKI remain unclear. This study aimed to explore the potential role and mechanism of isorhamnetin in inhibiting macrophage related inflammation and improving AKI injury. METHODS: We established an AKI mouse model by intraperitoneal injection of cisplatin in vivo, and constructed an inflammatory cell model by stimulating RAW264.7 cells with LPS. Creatinine and urea nitrogen were measured to evaluate the changes of renal function in AKI mice. The changes of renal pathological structure were observed by H&E staining. The inflammatory factor-related proteins and RNA expression levels were detected by Western blot and real time PCR. RESULTS: Isorhamnetin protected the kidney from cisplatin induced AKI and significantly inhibited the mRNA and protein levels of inflammatory cytokines (IL-1ß, IL-6, and TNF-α) both in AKI kidney and LPS-stimulated RAW264.7 cells. Interestingly, the data also demonstrated that isorhamnetin significantly upregulated the expression of secretory leukocyte peptidase inhibitor (SLPI), an anti-inflammatory factor, in AKI kidney and LPS-stimulated macrophages, as well as inhibited the M1 macrophage and activated M2 macrophage in vitro. Blocking of SLPI by siRNA activated Mincle-associated inflammatory signaling in macrophages, and the inhibitory effect of isorhamnetin on inflammation was significantly attenuated. CONCLUSION: Isorhamnetin inhibits macrophage inflammation and protects kidney in AKI may be related to downregulating Mincle/Syk/NF-κB-maintained macrophage phenotype by activating SLPI.

Astaxanthin exerts an adjunctive anti-cancer effect through the modulation of gut microbiota and mucosal immunity.

This study aimed to investigate the function of gut microbiota in astaxanthin's adjuvant anticancer effects. Our prior research demonstrated that astaxanthin enhanced the antitumor effects of sorafenib by enhancing the body's antitumor immune response; astaxanthin also regulated the intestinal flora composition of tumor-bearing mice. However, it is presently unknown whether this beneficial effect is dependent on the gut microbiota. We first used broad-spectrum antibiotics to eradicate gut microbiota of tumor-bearing mice, followed by the transplantation of fecal microbiota. The results of this study indicate that the beneficial effects of astaxanthin when combined with molecular targeting are dependent on the presence of intestinal microbiota. Astaxanthin facilitates the infiltration of CD8+ T lymphocytes into the tumor microenvironment and increases Granzyme B production by modulating the intestinal flora. Therefore, it strengthens the body's anti-tumor immune response and synergistically boosts the therapeutic efficacy of drugs. Astaxanthin stimulates the production of cuprocytes and mucus in the intestines by promoting the proliferation of Akkermansia. In addition, astaxanthin enhances the intestinal mucosal immunological function. Our research supports the unique ability of astaxanthin to sustain intestinal flora homeostasis and its function as a dietary immune booster for individuals with tumors.

Astaxanthin slows down skeletal muscle atrophy in H22 tumor-bearing mice during sorafenib treatment by modulating the gut microbiota.

Astaxanthin is a carotenoid that is taken orally and has antitumor and anti-inflammatory properties. Our previous research demonstrated that astaxanthin alleviated skeletal muscle atrophy during sorafenib treatment in H22 tumor-bearing mice and altered the intestinal flora composition. However, the relationship between astaxanthin's amelioration of skeletal muscle atrophy in tumor-bearing mice and its ability to regulate intestinal flora is not clear. We used broad-spectrum antibiotics to create pseudo-sterile tumor-bearing mice, which we then used in fecal bacteria transplantation experiments. Our results indicate that the role of astaxanthin in ameliorating skeletal muscle atrophy during molecularly targeted therapy in mice with tumors is dependent on the intestinal flora. Astaxanthin substantially promoted the proliferation of Blautia, Parabacteroides, and Roseburia, altered the levels of metabolites in mouse serum, and primarily affected the amino acid metabolism of mice. Astaxanthin ameliorated skeletal muscle atrophy by promoting the activation of AKT/FOXO3a, which inhibited the expression of ubiquitination-degrading Fbx32 and MuRF1 and promoted myogenesis in skeletal muscle. Our study confirms that the intestinal flora is an important target for astaxanthin to combat skeletal muscle atrophy. Our research supports the use of astaxanthin as a nutritional supplement and intestinal microecological regulator for cancer patients.

Virtual Reality in Clinical Nursing Practice Over the Past 10 Years: Umbrella Review of Meta-Analyses.

Background: Virtual reality (VR) has shown promising levels of effectiveness in nursing education, pain management, and rehabilitation. However, meta-analyses have discussed the effects of VR usage in nursing unilaterally and inconsistently, and the evidence base is diffuse and varied. Objective: We aimed to synthesize the combined evidence from meta-analyses that assessed the effects of nurses using VR technology on nursing education or patient health outcomes. Methods: We conducted an umbrella review by searching for meta-analyses about VR intervention in clinical nursing practice on Web of Science, Embase, Cochrane, and PubMed, and in reference lists. Eligible studies were published in English between December 1, 2012, and September 20, 2023. Meta-analyses of ≤2 intervention studies and meta-analyses without 95% CI or heterogeneity data were excluded. Characteristic indicators, population information, VR intervention information, and 95% CIs were extracted. A descriptive analysis of research results was conducted to discern relationships between VR interventions and outcomes. I2 and P values were used to evaluate publication bias. AMSTAR (A Measurement Tool to Assess Systematic Reviews) 2 and the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) checklist were used to appraise literature quality. Results: In total, 768 records were identified; 74 meta-analyses were included for review. The most reported VR study conditions were neuronursing (25/74, 34%), pediatric nursing (13/74, 18%), surgical and wound care (11/74, 15%), oncological nursing (11/74, 15%), and older adult nursing (10/74, 14%). Further, 30% (22/74) of meta-analyses reported publication bias, and 15% (11/74) and 8% (6/74) were rated as "high" based on AMSTAR 2 and the GRADE checklist, respectively. The main outcome indicators among all included meta-analyses were pain (37/214, 17.3%), anxiety (36/214, 16.8%), cognitive function (17/214, 7.9%), balance (16/214, 7.5%), depression (16/214, 7.5%), motor function (12/214, 5.6%), and participation in life (12/214, 5.6%). VR treatment for cognition, pain, anxiety, and depression was effective (all P values were <.05), while the utility of VR for improving motor function, balance, memory, and attention was controversial. Adverse effects included nausea, vomiting, and dizziness (incidence: range 4.76%-50%). The most common VR platforms were Pico VR glasses, head-mounted displays, the Nintendo Wii, and the Xbox Kinect. VR intervention duration ranged from 2 weeks to 12 months (typically ≥4 wk). VR session length and frequency ranged from 5 to 100 minutes and from 1 to 10 times per week, respectively. Conclusions: VR in nursing has positive effects-relieving patients' pain, anxiety, and depression and improving cognitive function-despite the included studies' limited quality. However, applying VR in nursing to improve patients' motor function, balance, memory, and attention remains controversial. Nursing researchers need to further explore the effects and standard operation protocols of VR in clinical practice, and more high-quality research on VR in nursing is needed.

VCAM-1 Promotes Angiogenesis of Bone Marrow Mesenchymal Stem Cells Derived from Patients with Trauma-Induced Osteonecrosis of the Femoral Head by Regulating the Apelin/CCN2 Pathway.

Trauma-induced osteonecrosis of the femoral head (TI-ONFH) is a pathological process in which the destruction of blood vessels supplying blood to the femoral head causes the death of bone tissue cells. Vascular cell adhesion molecule 1 (VCAM-1) has been shown to have potent proangiogenic activity, but the role in angiogenesis of TI-ONFH is unclear. In this work, we discovered that VCAM-1 was significantly downregulated in the bone marrow mesenchymal stem cells (BMSCs) derived from patients with TI-ONFH. Subsequently, we constructed BMSCs overexpressing VCAM-1 using a lentiviral vector. VCAM-1 enhances the migration and angiogenesis of BMSCs. We further performed mRNA transcriptome sequencing to explore the mechanisms by which VCAM-1 promotes angiogenesis. Gene ontology biological process enrichment analysis demonstrated that upregulated differentially expressed genes (DEGs) were related to blood vessel development. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that upregulated DEGs were engaged in the Apelin signaling pathway. Apelin-13 is the endogenous ligand of the APJ receptor and activates this G protein-coupled receptor. Treatment with Apelin-13 activated the Apelin signaling pathway and suppressed the expression of cellular communication network factor 2 in BMSCs. Furthermore, Apelin-13 also inhibits the migration and angiogenesis of VCAM-1-BMSCs. In summary, VCAM-1 plays an important role in vascular microcirculation disorders of TI-ONFH, which provides a new direction for the molecular mechanism and treatment of TI-ONFH.

Dietary supplementation with astaxanthin enhances anti-tumor immune response and aids the enhancement of molecularly targeted therapy for hepatocellular carcinoma.

Astaxanthin is a naturally occurring compound that possesses immunomodulatory properties. The results of our previous investigation indicated that astaxanthin has the potential to augment the anticancer effectiveness of the targeted medication sorafenib. However, the precise molecular mechanism underlying this phenomenon remains unclear. H22 tumor-bearing mice were treated with sorafenib at 30 mg kg-1 per day and their diet was supplemented with 60 mg kg-1 day-1 astaxanthin orally for a period of 18 days. The study revealed that the addition of astaxanthin to the diet facilitated the transition of tumor-associated macrophages from the M2 phenotype to the M1 phenotype. The application of astaxanthin resulted in an augmentation of CD8+ T cell infiltration within the tumor microenvironment through the activation of the CXCL9/CXCR3 signaling axis. Astaxanthin was found to enhance the production of cytokines that possess antitumor properties, including Granzyme B. Furthermore, the administration of astaxanthin resulted in alterations to the intestinal microbiota in H22-bearing mice, leading to the growth of bacteria that possess anti-tumor immune properties, such as Akkermansia. The findings of these studies indicate that astaxanthin has the potential to augment the immune response against tumors when used in conjunction with sorafenib. These studies offer a novel framework for the advancement of astaxanthin as an immunomodulatory agent and a dietary supplement for individuals with tumors.

Clinical features and prognosis of patients with metastatic ocular and orbital melanoma: A bi-institutional study.

PURPOSE: Metastatic ocular and orbital melanomas are extremely rare. The clinical characteristics and standard treatments for these patients are not fully established. MATERIALS AND METHODS: We retrospectively analyzed patients with metastatic ocular and orbital melanoma from Fudan University Shanghai Cancer Center and Eye & ENT Hospital of Fudan University between January 2012 and May 2022. RESULTS: Overall, 51 patients with metastatic ocular and orbital melanoma were included. The most common primary sites were uvea (73%), followed by conjunctiva (22%), lacrimal sac (4%), and orbit (2%). Patients with uveal melanoma (UM) had a significantly younger age (48 vs. 68 years, p < 0.001), higher incidence of liver metastases (89% vs. 9%, p<0.001), a lower incidence of lymph nodes metastases (16% vs. 46%, p = 0.043) and a lower incidence of BRAF mutation (0% vs. 55%, p<0.001) compared with patients with conjunctival melanoma (CM). The overall response rate of the first-line treatment was 18%. Three of the four patients with BRAF-mutated CM responded to dabrafenib and trametinib treatment. The median progression-free survival (PFS) and overall survival (OS) of first-line treatment were 5.1 and 11.9 months, respectively. Among patients with liver metastases, liver-directed treatment was correlated with better patient PFS (p < 0.001) and OS (p < 0.001) after adjusting for number of metastatic sites and primary sites. CONCLUSION: CM and UM have different characteristics. Patient with CM had a high incidence of BRAF mutation, and the treatment of BRAF and MEK inhibitors conferred clinical benefit. Liver directed therapies had a potential benefit in disease control in patients with liver metastases.

Preliminary proteomic analysis of human tears in lacrimal adenoid cystic carcinoma and pleomorphic adenoma.

AIM: To detect proteomic differences in tears between adenoid cystic carcinoma (ACC) and pleomorphic adenoma (PA). METHODS: Tear samples were collected from 4 patients with ACC, 5 with PA, and 4 control cases. Label-free analysis and parallel reaction monitoring (PRM) were used to screen and validate the tear proteome. Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) were conducted for bioinformatics analysis. RESULTS: In total, 1059 proteins in tear samples were identified by label-free analysis. Between ACC and PA, 415 differentially expressed proteins were detected. Based on the GO annotation, enzyme regulator activity and serine-type endopeptidase inhibitor activity in the molecular function category, blood microparticle and extracellular matrix in the cellular component category, and response to nutrient levels in the biological process category were most predominant. By KEGG pathway annotation, the different proteins between ACC and PA mainly participated in complement and coagulation cascades, amoebiasis, African trypanosomiasis and cholesterol metabolism. Eight proteins with mostly significant differences were verified by PRM, and five proteins with more than 10-fold increases in ACC compared with PA, including integrin ß, α-2-macroglobulin, epididymal secretory sperm binding protein Li 78p, RAB5C, and complement C5, were identified. CONCLUSION: The combined tools of label-free analysis and PRM are very effective and efficient, especially for samples such as tears. Some proteomic differences in tears between ACC and PA are identified and these protein candidates may be specific biomarkers for future exploration.

Low miR-182-5p Expressing Extracellular Vesicles Derived From Human Bone Marrow Stromal Cells of Subjects With Steroid-Induced Osteonecrosis of the Femoral Head Aggravate Disease Progression.

Steroid-induced osteonecrosis of the femoral head (SONFH) is a refractory, progressive disease. However, the underlying mechanisms that aggravate femoral head necrosis remain unclear. Extracellular vesicles (EVs) act as molecular carriers in intercellular communication. We hypothesize that EVs derived from human (h) bone marrow stromal cells (BMSC) resident in SONFH lesion areas promote the pathogenesis of SONFH. In the present study, we determined the modulatory effects of SONFH-hBMSCs-derived EVs on the pathogenesis of SONFH in vitro and in vivo. We found that the expression of hsa-miR-182-5p was downregulated in SONFH-hBMSCs and EVs isolated from those hBMSCs. After tail vein injection, EVs isolated from hBMSCs transfected with hsa-miR-182-5p inhibitor aggravated femoral head necrosis in the SONFH mouse model. We conclude that miR-182-5p regulates bone turnover in the SONFH mouse model via targeting MYD88 and subsequent upregulation of RUNX2 expression. We further assume that EVs derived from hBMSCs resident in SONFH lesion areas aggravate femoral head necrosis by downregulating miR-182-5p secreted from hBMSC located outside these lesions. We suggest that miR-182-5p could provide a novel target for future therapeutic approaches to treat or prevent SONFH. © 2023 American Society for Bone and Mineral Research (ASBMR).

Inflammatory Cytokine Interleukin-6 (IL-6) Promotes the Proangiogenic Ability of Adipose Stem Cells from Obese Subjects via the IL-6 Signaling Pathway.

BACKGROUND: The prevalence of obesity, as well as obesity-induced chronic inflammatory diseases, is increasing worldwide. Chronic inflammation is related to the complex process of angiogenesis, and we found that adipose-derived stem cells from obese subjects (obADSCs) had proangiogenic features, including higher expression levels of interleukin-6 (IL-6), Notch ligands and receptors, and proangiogenic cytokines, than those from control subjects. We hypothesized that IL-6 and Notch signaling pathways are essential for regulating the proangiogenic characteristics of obADSCs. OBJECTIVE: This study aimed to investigate whether the inflammatory cytokine interleukin 6 (IL-6) promotes the proangiogenic capacity of adipose stem cells in obese subjects via the IL-6 signaling pathway. METHODS: We compared the phenotype analysis as well as cell doubling time, proliferation, migration, differentiation, and proangiogenic properties of ADSCs in vitro. Moreover, we used small interfering RNAs to inhibit the gene and protein expression of IL-6. RESULTS: We found that ADSCs isolated from control individuals (chADSCs) and obADSCs had similar phenotypes and growth characteristics, and chADSCs had a stronger differentiation ability than obADSCs. However, obADSCs were more potent in promoting EA.hy926 cell migration and tube formation than chADSCs in vitro. We confirmed that IL-6 siRNA significantly reduced the transcriptional level of IL-6 in obADSCs, thereby reducing the expression of vascular endothelial growth factor (VEGF)- A, VEGF receptor 2, transforming growth factor ß, and Notch ligands and receptors in obADSCs. CONCLUSION: The finding suggests that inflammatory cytokine interleukin-6 (IL-6) promotes the proangiogenic ability of obADSCs via the IL-6 signaling pathway.

Network and Experimental Pharmacology to Decode the Action of Wendan Decoction Against Generalized Anxiety Disorder.

Objective: The mechanism of Wendan Decoction (WDD) against Generalized Anxiety Disorder (GAD) was predicted by network pharmacology and validated by in vivo and in vitro experiments. Methods: The targets of WDD for the treatment of GAD were obtained by a search of online databases. Further, PPI network and KEGG enrichment were used to identify the key targets and pathways. Ultimately, these key targets and pathways were validated by in vivo experiments on GAD mice modeled by repeated restraint stress (RRS) and in vitro experiments on inflammatory factor stimulated BV-2 cells. Results: Through searching the databases, the 137 ingredients of WDD that correspond to 938 targets and 4794 targets related to GAD were identified. Among them, 569 overlapping targets were considered as the therapeutic targets of WDD for GAD. PPI analysis showed that the inflammation-related proteins IL-6, TNF, SRC and AKT1 were the key targets, and KEGG enrichment suggested that PI3K/AKT and MAPK signaling pathways were key pathways of WDD in the treatment of GAD. In vivo experiments, RRS mice exhibited abnormality in behavioristics in open field test (OFT) and elevated plus maze (EPM) and increases in serum corticosterone and the percentage of lymphocytes positive for IL-6 in peripheral blood. These abnormal changes can be reversed by WDD and the positive control drug paroxetine. In vitro experiments, WDD can inhibit IL-6 induced activation of PI3K/AKT and MAPK signaling pathways in BV2 cells, and suppress the ensuing release of inflammatory factors TNF-α, IL-1ß and PGE2, and showed a dose-dependent effect. Conclusion: WDD is able to resist GAD by relieving inflammatory response in peripheral and central system.

Lacrimal sac lymphoma: a case series and literature review.

AIM: To study the clinical and pathological characteristics of the lacrimal sac lymphoma, which is rare but it is the major type of non-epithelial malignant tumor in the lacrimal sac region. METHODS: Sixty-four cases of malignant lacrimal sac tumors in our hospital from 1986 to 2020 were retrospectively reviewed. Eight cases of lacrimal sac lymphoma were carefully reviewed. RESULTS: There were five mucosal-associated lymphoid tissue (MALT) lymphomas, one diffused large B-cell lymphoma, one NK/T cell lymphoma, and one mantle cell lymphoma. All eight patients represented symptoms of epiphora with swelling in the lacrimal sac for a certain period of time and showed no signs of systemic involvement at the first time of clinical visits. They had received either chemotherapy or radiotherapy after surgery. Long-term follow-up (from 11 to 220mo) showed that, except one patient with MALT lymphoma died for unknown reasons at 104mo after surgery, the other 7 patients were all alive with no signs of local recurrence, neither in other organs. CONCLUSION: Non-epithelial malignant tumors of the lacrimal sac are rare and lymphoma is the major subtype.

Preoperative evaluation of endoscopic submucosal dissection for early gastric cancer.

OBJECTIVE: To retrospectively analyze the preoperative endoscopic evaluation of the size, nature, and depth of lesions in endoscopic submucosal dissection (ESD) for early gastric cancer and precancerous lesions, determine whether the lesions can be completely resected, and reduce the risk of additional surgery after ESD. METHODS: A total of 114 patients with high-grade intraepithelial neoplasia(HGIN) and early gastric cancer treated with ESD in Hebei General Hospital from January 2016 to April 2021 were enrolled in this study. The lesions were evaluated preoperatively according to the endoscopic findings of white light, magnifying endoscopy, endoscopic features of narrow band imaging, and preoperative pathology. Lesion size, positive resection margin, lesion depth, and vascular invasion of postoperative pathology were used as criteria. RESULTS: There were 121lesions in 114 patients. The coincidence rates of preoperative and postoperative pathology were 87.21% (75/86) for HGIN and 92.1% (35/38) for adenocarcinoma. There was no significant difference in the coincidence rate between preoperative pathological evaluation and postoperative pathology among the 3 lesions (χ2 = 10.614, P = .005). The type and malignancy of the lesion were not related to its location or size. Magnifying endoscopy combined with narrow-band imaging showed that HGIN and early gastric cancer had clear borders, irregular microvessels, and irregular surface microarchitecture on endoscopic features. Lesions > 3 cm, surface ulcers and spontaneous bleeding may be risk factors for deeper lesions. CONCLUSION: ESD is not only a method for the treatment of early gastric cancer and precancerous lesions, but is also an important method for definite pathological diagnosis. Accurate preoperative assessment of lesion type, lesion extent and depth of invasion is helpful to improve the complete resection rate of ESD and reduce the risk of additional surgery.

Transmissible Endoplasmic Reticulum Stress Mediated by Extracellular Vesicles from Adipocyte Promoting the Senescence of Adipose-Derived Mesenchymal Stem Cells in Hypertrophic Obesity.

Hypertrophic obesity, characterized by an excessive expansion of subcutaneous adipocytes, causes chronic inflammation and insulin resistance. It is the primary feature of obesity in middle-aged and elderly individuals. In the adipose microenvironment, a high level of endoplasmic reticulum (ER) stress and changes in the extracellular vesicle (EV) composition of adipocytes may cause the senescence and restrained differentiation of progenitor cells of adipose, including adipose-derived mesenchymal stem cells (ASCs). In this study, a hypertrophic obesity mouse model was established, and the effects of adipocytes on the ER stress and senescence of ASCs were observed in a coculture of control ASCs and hypertrophic obesity mouse adipocytes or their derived EVs. The adipocytes of hypertrophic obesity mice were treated with GW4869 or an iron chelation agent to observe the effects of EVs secreted by adipocytes and their iron contents on the ER stress and senescence of ASCs. Results showed higher ER stress level and senescence phenotypes in the ASCs from the hypertrophic obesity mice than in those from the control mice. The ER stress, senescence phenotypes, and ferritin level of ASCs can be aggravated by the coculture of ASCs with adipocytes or EVs released by them from the hypertrophic obesity mice. GW4869 or iron chelator treatment improved the ER stress and senescence of the ASCs cocultured with EVs released by the adipocytes of the hypertrophic obesity mice. Our findings suggest that EV-mediated transmissible ER stress is responsible for the senescence of ASCs in hypertrophic obesity mice.

A Novel and Easy-to-Promote Prognostic Model for Patients With Uveal Melanoma.

Purpose: To establish an easy and widely applicable prognostic prediction model for uveal melanoma (UM) based on a Chinese population. Patients and Methods: A total of 295 consecutive cases treated at the Eye & ENT Hospital of Fudan University were included as the primary cohort, and 256 cases were included in the validation cohorts from two external Caucasian databases. Clinicopathological data were collected retrospectively, and nomogram models were formulated based on multivariable analysis. The concordance index (C-index), AUC (area under the Receiver Operating Characteristic, ROC curve), and Brier score were calculated and compared. Results: Based on the training cohort, a nomogram model was established with five relevant variables: age, tumor size, ciliary body involvement, non-spindle cell type and extra-scleral extension. The C-index was 0.737, the 3- and 5-year AUCs were 0.767 and 0.742, and the Brier scores for 3- and 5-year survival were 0.082 and 0.129, respectively, which showed superior prediction compared to that of the Tumor, Node and Metastasis staging system. The model also displayed good discrimination and calibration in the external validation cohorts. By risk stratification, patients could be divided into low- and high-risk groups, and the overall survival curves displayed significant differences in the training and validation cohorts. Conclusion: Our nomogram model was simple and accurate at predicting the overall survival of patients with UM. It was established based on Asian patients and proved suitable for Caucasian patients; thus, it has a wide range of potential applications, especially for patients living in less medically developed countries and regions.