A real-time video-based social network platform for online ultrasound education.

BACKGROUND: In the post-pandemic era, traditional methods of professional development for ultrasound practitioners are insufficient, and it is therefore imperative to explore a new avenue for continuing education. This article explores the role of the real-time video-based social networks for medicine combined with e-enterprise to train ultrasound practitioners. METHODS: We created a live broadcasting room on the real-time video-based social networks for medicine and imparted online education on ultrasound usage with "YiQixiu" as the transmission carrier. We developed a satisfaction questionnaire for the online class in real time, and tested the validity and reliability of the questionnaire. Descriptive statistical analysis was used (P ≤ 0.05 indicates significance). RESULTS: The landing page on YiQixiu was mainly concentrated in the Hunan Province, accounting for 56% of visitors. The total number of people watching online real-time lectures was 32,344; the maximum number of fixed attendance was 17,000, and the minimum number was 3,000. The questionnaire met the needs of this study, with a reliability value of 0.93. The participants were from 18 provinces, 4 autonomous regions, and 4 municipalities directly under the central government. CONCLUSION: The real-time video-based social networks for medicine combined with the YiQixiu live platform is a good method for imparting ultrasound medical education online.

Volume and function changes of left atrium and left ventricle in patients with ejection fraction preserved heart failure measured by a three dimensional dynamic heart model.

The accurate diagnosis of HFpEF is still challenging and controversial. In this study, we used 3D-DHM technology to compare the differences of cardiac structure and function between HFpEF patients and healthy controls, as well as the differences of two-dimensional and three-dimensional cardiac function in HFpEF patients. Echocardiography with 3D-DHM and conventional two-dimensional (2D) methods were applied to measure the volume and function parameters of left atrium and ventricle of patients with HFpEF and healthy controls. Significant differences of 3D cardiac function indexes including LVESV, 3D-LVEF, ESL, SV, CI, EDmass, LAVmax, LAVmin, LAEF, and LAVI were observed between patients with HFpEF and controls (P < 0.05). However, no significant difference of LVEDV and EDL were observed (P > 0.05). In addition, we found no significant between-group difference in 2D cardiac function indexes such as LVDD and 2D-LVEF (P > 0.05), but the LAD, LVSD, LVPW, IVS, E, E/A, and E/e ' were significantly different between groups (P < 0.05). There was no significant difference between 3D-LVEF and 2D-LVEF in the control group (P > 0.05), while 3D-LVEF in the HFpEF group was lower than 2D-LVEF(P < 0.05). Among the two-dimensional and three-dimensional parameters of HFpEF patients, the parameters related to diastolic function changed more significantly than those of the normal group, and the three-dimensional LVEF of HFpEF patients decreased. The three-dimensional cardiac function parameters analyzed by DHM can provide more information regarding myocardial mechanics.

A Foundation Model for Cell Segmentation.

Cells are a fundamental unit of biological organization, and identifying them in imaging data - cell segmentation - is a critical task for various cellular imaging experiments. While deep learning methods have led to substantial progress on this problem, most models in use are specialist models that work well for specific domains. Methods that have learned the general notion of "what is a cell" and can identify them across different domains of cellular imaging data have proven elusive. In this work, we present CellSAM, a foundation model for cell segmentation that generalizes across diverse cellular imaging data. CellSAM builds on top of the Segment Anything Model (SAM) by developing a prompt engineering approach for mask generation. We train an object detector, CellFinder, to automatically detect cells and prompt SAM to generate segmentations. We show that this approach allows a single model to achieve human-level performance for segmenting images of mammalian cells (in tissues and cell culture), yeast, and bacteria collected across various imaging modalities. We show that CellSAM has strong zero-shot performance and can be improved with a few examples via few-shot learning. We also show that CellSAM can unify bioimaging analysis workflows such as spatial transcriptomics and cell tracking. A deployed version of CellSAM is available at https://cellsam.deepcell.org/.

AGAP2-AS1/BRD7/c-Myc signaling axis promotes skin cutaneous melanoma progression.

OBJECTIVE: To examine the effects and mechanisms of AGAP2 Antisense RNA 1 (AGAP2-AS1) in progression of skin cutaneous melanoma (SKCM). METHODS: AGAP2-AS1 expression and SKCM survival outcomes were assessed using bioinformatics analysis. In vitro and in vivo assays, including cell proliferation, colony formation, migration, and tumor formation assays, were performed to detect AGAP2-AS1 oncogenic effects in SKCM. RNA pull-down, RNA immunoprecipitation (RIP), and co-immunoprecipitation were used to evaluate the mechanism of AGAP2-AS1 in SKCM progression. RESULTS: AGAP2-AS1 was upregulated in human SKCM tissues and cells and predicted a worse prognosis. AGAP2-AS1 silencing in two SKCM cell lines inhibited cell proliferation, as well as colony formation and migration both in vitro and in vivo. The RNA pull-down assay and RIP analysis results indicated that AGAP2-AS1 interacted with bromodomain containing 7 (BRD7). AGAP2-AS1 knockdown attenuated the BRD7 and c-Myc interaction, which reduced c-Myc expression. The altered phenotypes found in AGAP2-AS1- and BRD7-deficient cells were rescued by overexpression of c-Myc. CONCLUSIONS: AGAP2-AS1 participated in oncogenesis in SKCM via the BRD7/c-Myc signaling pathway. These results suggest a molecular mechanism for AGAP2-AS1 in the carcinogenesis of SKCM.

Identification of a ferroptosis- and oxidative stress-associated gene signature for prognostic stratification of ovarian cancer.

BACKGROUND: Studies have shown that ferroptosis- and oxidative stress-related genes (FORGs) perform crosstalk in ovarian cancer (OC). The specific role of FORGs in OC, however, remains unclear. We aimed to develop a molecular subtype and prognostic model associated with FORGs that could predict OC prognosis and evaluate the infiltration of tumor-associated immune cells. METHODS: Gene expression samples were collected from the GEO (GSE53963) and Cancer Genome Atlas (TCGA) databases. Kaplan-Meier analysis was used to evaluate prognostic efficacy. Unsupervised clustering was applied to identify molecular subtypes, which was followed by tumor immune cell infiltration and functional enrichment analyses. Subtype-related differentially expressed genes (DEGs) were identified and used to establish prognostic models. Associations between the model and immune checkpoint expression, stromal scores, and chemotherapy were investigated. RESULTS: OC patients were categorized into two FORG subtypes based on the expression characteristics of 19 FORGs. Molecular subtypes associated with patient prognosis, immune activity, and energy metabolism pathways were identified. Subsequently, DEGs in the two FORG subtypes were identified and used in prognostic models. We identified six signature genes (MEGF8, ECE1, SASH1, ARHGEF16, PLXNA1, and FCGBP) with LASSO analysis to assess the risk of OC. Patients in the high-risk group had poor prognoses and immunosuppression, while the risk scores were significantly associated with immune checkpoint expression, stromal scores, and chemotherapy sensitivity. CONCLUSIONS: Our novel clustering algorithm was used to create distinct clusters of OC patients and a prognostic model was developed that accurately predicted patient outcomes and chemotherapy responses. This approach offers effective precision medicine for OC patients.

Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/ß-catenin pathway.

As a common malignant tumor among women, ovarian cancer poses a serious threat to their health. This study demonstrates that long non-coding RNA NRSN2-AS1 is over-expressed in ovarian cancer tissues using patient sample and tissue microarrays. In addition, NRSN2-AS1 is shown to promote ovarian cancer cell proliferation and metastasis both in vitro and in vivo. Mechanistically, NRSN2-AS1 stabilizes protein tyrosine kinase 2 (PTK2) to activate the ß-catenin pathway via repressing MG-53-mediated ubiquitinated degradation of PTK2, thereby facilitating ovarian cancer progression. Rescue experiments verify the function of the NRSN2-AS1/PTK2/ß-catenin axis and the effects of MG53 on this axis in ovarian cancer cells. In conclusion, this study demonstrates the key role of the NRSN2-AS1/PTK2/ß-catenin axis for the first time and explores its potential clinical applications in ovarian cancer.

An Integrative Transcriptomic Analysis Reveals EGFR Exon-19 E746-A750 Fragment Deletion Regulated miRNA, circRNA, mRNA and lncRNA Networks in Lung Carcinoma.

Introduction: Competing endogenous RNA (ceRNA) appears to be an important post-transcriptional manner that regulates gene expression through a miRNA-mediated mechanism. Mutations in exon-19 of EGFR were frequently observed in lung cancer genes, which were associated with EGFR activity and EGFR-targeted therapies. Methods: We explored the transcriptome regulated by mutation in EGFR exon-19 E746-A750 fragment via using a network modeling strategy. We applied transcriptome sequencing to detect the deletion process of EGFR exon-19 E746-A750 fragment. Bio-informatics analyses were used to predict the gene target pairs and explain their potential roles in tumorigenesis and progression of lung cancer. Results: We conducted an explorative lncRNA/miRNA/circRNA and mRNA expression study with two groups of lung adenocarcinoma tissues, including EGFR exon-19 E746-A750 deletion group and EGFR exon-19 wild-type group. Meanwhile, we screen out the hub genes related to the EGFR-19-D patient. Significant pathways and biological functions potentially regulated by the deregulated 128 non-coding genes were enriched. Conclusion: Our work provides an important theoretical, experimental and clinical foundation for further research on more effective targets for the diagnosis, therapy and prognosis of lung cancer.

Measuring of strain parameters reflects changes of right ventricular function before and after thrombolytic therapy in patients with acute pulmonary embolism.

Strain parameters on speckle tracking echocardiography (STE) have been proposed as effective indexes for evaluating right ventricular (RV) function. This pilot study investigated the role of STE-derived strain parameters in assessing global and regional RV myocardial mechanical changes in patients with acute pulmonary embolism (PE) before and after thrombolytic therapy. In this case-control study, a total of 73 PE patients, 34 with pulmonary hypertension (PH) and 39 without PH, who underwent thrombolytic therapy were included. Healthy volunteers were included as controls. The peak longitudinal systolic strain (PLSS) and time to PLSS (TTP) for the global and regional RV were analyzed by STE software immediately before and 14 days after thrombolytic therapy. Changes in STE-derived strain parameters and conventional ultrasound parameters were compared. PLSS and TTP decreased before treatment in PE patients compared with measurements in the control group, particularly in those with PH. Also, the strain parameters decreased more significantly for the free wall than for the septum wall (P < 0.05). Moreover, the RV diastolic diameter (RVDD) and RV/left ventricular (LV) diameter ratio increased, while RV fraction shortening (RVFS), RV fractional area change (RVFAC), tricuspid regurgitation pressure gradient (TRPG), and tricuspid annular peak systolic excursion (TAPSE) decreased (P < 0.05). The global strain parameters for the RV were positively correlated with RVDD and RV/LV diameter ratio, but negatively correlated with RVFS, RVFAC, TRPG, and TAPSE (P < 0.05). After treatment, the strain parameters differed significantly between PE patients with PH and controls but did not differ between PE patients without PH and controls. STE-derived parameters are effective for detecting changes in global and regional RV function in PE patients with or without acute PH.

Long non-coding RNA DEPDC1-AS1 promotes proliferation and migration of human gastric cancer cells HGC-27 via the human antigen R-F11R pathway.

OBJECTIVE: Long non-coding (lnc) RNAs are critical regulators in carcinogenesis. The novel lncRNA DEPDC1 antisense RNA 1 (DEPDC1-AS1) was recently associated with poor prognosis in triple-negative breast cancer and lung adenocarcinoma. However, its role in regulating the malignant progression of gastric cancer (GC) and its molecular mechanism are unclear. We herein explored the functions of DEPDC1-AS1 in GC progression. METHODS: DEPDC1-AS1 expression and prognosis in GC tissues were examined by bioinformatics analysis and quantitative reverse transcription polymerase chain reaction. The DEPDC1-AS1 function in GC cells was explored by the cell counting kit-8 assay, colony formation assay, Transwell assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, 5-ethynyl-2'-deoxyuridine-incorporation, and the xenograft tumor model. The DEPDC1-AS1 and human antigen (Hu)R interaction was determined by RNA pull-down and RNA immunoprecipitation. RESULTS: DEPDC1-AS1 was overexpressed in GC tissues and cell lines, and associated with a worse prognosis in GC patients. In vitro and in vivo assays showed that DEPDC1-AS1 promoted HGC-27 cell proliferation and migration. Mechanistically, DEPDC1-AS1 served as a scaffold by combining with HuR to target the specific mRNA F11R. CONCLUSION: DEPDC1-AS1 plays a crucial role in GC development and progression and is a potential biomarker for the early detection or prognosis of GC.

Testis-enriched Asb12 is not required for spermatogenesis and fertility in mice.

Background: Members of the ankyrin repeat and SOCS box (Asb) family are expressed abundantly in testes. Some Asb genes/proteins are required for spermatogenesis, but the function of Asb12 during spermatogenesis is not clear. We investigated the physiological role of Asb12 in murine testes. Methods: The clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 system was used to generate Asb12-knockout (KO) mice. Histology and immunostaining were done to assess the effects of Asb12 KO on mouse testes and epididymides. Semen quality was analyzed using a computer-assisted sperm analyzer. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling assay was employed to examine testicular apoptosis. Real-time reverse transcription-quantitative polymerase chain reaction (PCR) was conducted to calculate gene transcription levels. Results: Asb12 was expressed predominantly in murine testes. Immunostaining of Asb12 protein revealed that Asb12 was located specifically in the acrosome of elongated spermatids, which suggested a potential role of Asb12 during spermatogenesis. However, Asb12-KO mice had normal fertility, and no overt difference was detected in testicular morphology, semen quality, or apoptosis when comparing Asb12-KO and Asb12-wild type (WT) mice. Gene expression of several Asb family members was increased significantly in the testes of Asb12-KO mice when compared with that in Asb12-WT mice, which suggested functional compensation from paralogs for Asb12 loss. Conclusions: We demonstrated that Asb12 is not essential for the spermatogenesis and fertility of mice. Our findings will assist researchers in avoiding redundant efforts, and provide a baseline resource for genetic studies on human fertility.

Twist/untwist parameters are promising evaluators of myocardial mechanic changes in heart failure patients with preserved ejection fraction.

BACKGROUND: This study aimed to evaluate the twist/untwist parameters of the left ventricle (LV) in patients with heart failure with preserved ejection fraction (HFpEF) measured by ultrasonic two-dimensional speckle tracking echocardiography (STE) and to examine the correlations between twist parameters and serum N-terminal pro b-type natriuretic peptide (NT-proBNP) as well as conventional two-dimensional echocardiography (2DE) indexes. HYPOTHESIS: Changes in twist/untwist parameters can be used to evaluate LV function in HFpEF patients. METHODS: In 63 HFpEF patients and 40 healthy controls, we analyzed LV twist/untwist parameters by STE, cardiac function by 2DE, and serum NT-proBNP by enzyme-linked immunosorbent assay (ELISA). The correlations between twist/untwist parameters and 2DE parameters and serum NT-proBNP were examined by Pearson correlation analysis. RESULTS: Left ventricular end diastolic inner diameter and ejection fraction in HFpEF patients were within the normal range, whereas other 2DE parameters including left ventricular posterior wall end diastolic thickness, interventricular septal thickness, left atrial volume index, E, E/A, and E/e' differed significantly between HFpEF patients and control subjects. The twist/untwist parameters such as peak apical rotation (Par), peak untwisting velocity (PUWV), and isovolumic diastole untwisting percentage (Iutw%) were significantly decreased in HFpEF patients compared with control participants. Positive correlations between PUWV/Iutw% and E/A/E/e' and a significant negative correlation between PUWV/Iutw% and left atrial volume index (LAVI) were observed. The plasma NT-proBNP concentration was positively correlated with LAVI, but negatively correlated with PUWV and Iutw%. CONCLUSIONS: Changes in twist/untwist parameters correlate well with conventional 2DE parameters and plasma levels of NT-proBNP, and can be used to evaluate LV function in HFpEF patients. Par is sensitive to the LV myocardial function damage.

A Transcriptional Sequencing Analysis of Islet Stellate Cell and Pancreatic Stellate Cell.

BACKGROUND: Our previous studies have shown that islet stellate cell (ISC), similar to pancreatic stellate cell (PSC) in phenotype and biological characters, may be responsible for the islet fibrosis in type 2 diabetes. To further identify the differences between PSC and ISC and for better understanding of the physiological function of ISC, we employed genome-wide transcriptional analysis on the PSCs and ISCs of Wistar rats. METHOD: PSCs and ISCs from each rat were primarily cultured at the same condition. Genome-wide transcriptional sequence of stellate cells was generated. The identified differentially expressed genes were validated using RT-PCR. RESULTS: 32 significant differentially expressed genes between PSCs and ISCs were identified. Moreover, collagen type 11a1 (COL11A1), was found to be expressed 2.91-fold higher in ISCs compared with PSCs, indicating that COL11A1 might be a potential key gene modulating the differences between PSC and ISC. CONCLUSIONS: Our study identified and validated the differences between PSC and ISC in genome-wide transcriptional scale, confirming the assumption that ISC and PSC are similar other than identical. Moreover, our data might be instrumental for further investigation of ISC and islet fibrosis, and some differential expressed genes may provide an insight into new therapeutic targets for type 2 diabetes.

Effects of lidocaine on cerebral oxygen supply-consumption balance and hemodynamics during anesthesia induction in patients with supratentorial tumor.

OBJECTIVE: To study the effects of lidocaine on the balance between cerebral oxygen supply-consumption and on the hemodynamics during anesthesia induction in patients with supratentorial tumor. METHODS: Twenty-four patients with supratentorial tumor were randomly divided into lidocaine group (n=12) and control group (n=12). Blood gas analysis and determinations of plasma lactic acid and glucose in the radial artery and internal jugular venous bulb were performed. Oxygen extraction ratio (OER) and blood oxygen content in the artery and internal jugular venous bulb were calculated during anesthesia induction. RESULTS: OER and difference declined in plasma lactic acid level between the internal jugular venous bulb and the artery, and blood oxygen saturation as well as blood oxygen pressure in the internal jugular venous bulb and the artery increased along with blood oxygen content in the internal jugular venous bulb in both groups during anesthesia induction. Comparison between the groups showed that only the changes in blood oxygen pressure in the internal jugular venous bulb were statistically significant. Changes in the hemodynamics in lidocaine group were less obvious than those in the control group during anesthesia induction. CONCLUSION: Lidocaine does not significantly influence cerebral oxygen balance and may effectively inhibit hemodynamic response during anesthesia induction in patients with supratentorial tumor.