LncRNA DANCR upregulation induced by TUFT1 promotes malignant progression in triple negative breast cancer via miR-874-3p-SOX2 axis.

Triple negative breast cancer (TNBC) is a subtype of breast cancer with poorest survival outcome and is prone to metastasis. TUFT1 and the long non-coding RNA (lncRNA), DANCR, play vital roles in metastasis and progression of various cancers. However, the correlation between TUFT1 and DANCR in TNBC and their downstream molecular mechanisms are still undetermined. We demonstrated that upregulation of TUFT1 in TNBC was related to a worse survival in TNBC patients. The TNBC cells invasiveness was augmented by TUFT1 in a dose-dependent manner, while inhibiting TUFT1 repressed the invasiveness. Particularly, the expression of TUFT1 was positively correlated with the expression of DANCR in TNBC tissues. In addition, TUFT1 increased DANCR expression, while silencing DANCR ameliorated the invasiveness of TNBC cells induced by TUFT1. As demonstrated, TUFT1 interacted with miR-874-3p. Subsequently, qRT-PCR together with luciferase reporter further demonstrated that DANCR acted as competing endogenous (ceRNA) for miR-874-3p, thereby regulating the de-repression of SOX2 and advancing epithelial-mesenchymal transition (EMT) in TNBC. The present research shows that TUFT1 promotes the malignant development in TNBC via enhancing the expression of DANCR. The upregulation of DANCR may contribute to the progression and tumor invasiveness of TNBC, considering that DANCR functions as a miR-874-3p sponge, thus modulating SOX2 positively. Collectively, the present study explored the molecular mechanism underlying TUFT1 in TNBC, raising a TUFT1-mediated therapy for the treatment of patients with TNBC.

Charting the course of ferroptosis research in lung cancer: Insights from a bibliometric analysis.

Background: Lung cancer, a major cause of cancer-related mortality globally, necessitates innovative therapeutic strategies. Ferroptosis, an iron-dependent, non-apoptotic cell death form, has risen as a crucial therapeutic target. This study aims to conduct a comprehensive bibliometric analysis of ferroptosis in lung cancer, highlighting principal research trends, influential publications, and prospective future directions. Methods: This study utilized bibliometric tools such as VOSviewer, CiteSpace, and the R package "bibliometrix" to thoroughly analyze 488 articles on ferroptosis in lung cancer from 2014 to October 2023. Data from the Web of Science Core Collection were analyzed to determine spatial and temporal trends, identify prominent authors and seminal works, and uncover emerging hotspots and frontiers of the field. The literature was segmented into coherent thematic groups through cluster analysis. Results: Our analysis revealed a significant exponential growth in publications from 2019 to 2023, mirroring the increasing interest in this area. Predominantly, the influential research was published in high-impact journals, with Scott J. Dixon's works being the most cited. The study identified four primary research themes: Lung Cancer Specifics; Biomarker Identification and Prognosis; Cellular Death Mechanisms and Metabolic Regulation; and Cancer Stem Cells and Therapeutic Resistance. Recent studies have increasingly focused on areas such as the immune microenvironment and mitochondrial dysfunction. Furthermore, the analysis highlighted the field's global collaborative nature, with significant contributions from China, the USA, and Germany. Conclusion: This extensive bibliometric analysis emphasizes the growing importance of ferroptosis in lung cancer research. The identified themes and emerging topics underline the field's complexity and suggest new research avenues. This study promotes a holistic research approach, advocating for the exploration of innovative ferroptosis-targeting therapies that could revolutionize lung cancer treatment.

Mapping the lymph node metastasis landscape: A bibliometric Odyssey of papillary thyroid carcinoma publications (2012-2022).

Objective: Lymph node metastasis in papillary thyroid carcinoma (PTC) has become an area of great interest in the study of thyroid diseases. The aim of this study was to elucidate the research trends and impact of lymph node metastasis of PTC in the study of thyroid diseases through a comprehensive bibliometric analysis. Methods: We conducted an extensive bibliometric review of the literature on lymph node metastasis in PTC using the Web of Science Core Database (WOSCC), which included approximately 3292 publications from 2012 to 2022. Data analysis and visualization were performed, using advanced bibliometric tools including VOSviewer, CiteSpace, and bibliometrix R software packages. Results: A total of 3292 publications from 81 one countries were identified. The analysis showed a pattern of growth in the number of publications per year from 2012 to 2022, with China having the highest number of papers. Outstanding contributions were made by China, Korea, USA, Italy and Japan, with Thyroid being the most important journal. The author who published the most papers was Jingqiang Zhu. The institutions that published the most papers were Shanghai Jiao Tong University and Yonsei University. The analysis found that prognosis, recurrence, and ultrasound were the keywords with the highest frequency of occurrence in addition to those related to the title of this article. Conclusion: Our bibliometric analysis outlines the current state of research on lymph node metastasis in PTC, highlighting significant contributions, trends, and future research directions.

Cardiac self-limiting rhabdomyomas in a neonatal patient with tuberous sclerosis complex: a case report with negative genetic testing.

Background: Tuberous Sclerosis Complex (TSC) is a hereditary condition that leads to the development of non-malignant neoplasms in various organs, including cardiac rhabdomyomas, which can cause significant complications. Case presentation: This report describes the case of a 15-day-old male neonate who was hospitalized due to intracardiac masses and brain lesions, despite the absence of TSC gene mutations. The patient's mother exhibited facial angiofibromas, a common feature of TSC. Over a 2-year follow-up period, spontaneous regression of the cardiac tumor was observed. Conclusions: This case illustrates that not all TSC cases exhibit detectable TSC gene mutations. Current treatment strategies, such as mTOR inhibitors, offer potential effectiveness in managing associated cardiac rhabdomyomas. Further research should focus on evaluating the therapeutic potential of these inhibitors.

Case report: Surgical management of a rare right coronary artery fistula with a giant pseudoaneurysm compressing the pulmonary vein in a young patient.

Congenital coronary artery fistula (CAF) represents a remarkable rarity within the realm of cardiovascular anomalies, characterized by an aberrant connection between coronary arteries and either cardiac chambers or major vessels. Clinical manifestations of CAFs often remain unspecified or may even be entirely absent, posing diagnostic challenges. Notably, patients harboring substantial CAFs may exhibit symptoms such as palpitations, chest tightness, and dyspnea. Although right-sided congenital CAFs are relatively prevalent, the occurrence of a CAF accompanied by a colossal pseudoaneurysm imposing compression upon the pulmonary vein is an exceedingly rare phenomenon. This exceptional case report delineates a singular fistula originating from the right coronary artery, extending its course to the right atrium, and remarkably featuring a substantial pseudoaneurysm exerting compression upon the right superior pulmonary vein. Therapeutic intervention encompassed surgical closure of the proximal artery and excision of the pseudoaneurysm, underscoring the complexity and criticality of managing such intricate cardiac anomalies to ensure optimal patient outcomes.

Patients with New-Onset Tumor of Severe Coronary Artery Disease May be at a Higher Risk of Arrhythmia.

BACKGROUND: Arrhythmia is one of the causes of death in severe coronary artery disease patients who also suffered from cancer. Our research aims to compare the incidence of arrhythmia between severe coronary artery disease patient with and without new-onset tumor. Methodology. We enrolled 79 patients (December 2019-December 2020) with severe coronary artery disease in this study, and 40 of them were complicated with new-onset tumor. The details of all subjects were thoroughly obtained; the laboratory tests were implemented including creatinine before coronary angiography. The appraisal of the severity of coronary artery disease was applied by Gensini score. The cardiac inspection includes UCG, 12-lead ECG, and Holter monitor. RESULTS: Among them, there were 40 patients in the experimental group and 39 patients in the control group. The difference at the baseline between the two sets of figures was not statistically significant (P > 0.05). The incidence of arrhythmia between the two groups was statistically significant (P < 0.05). CONCLUSIONS: The incidence of arrhythmia in severe coronary artery disease patients who were complicated with new-onset tumor was higher than that in patients with severe coronary artery disease alone, and attention should be paid to arrhythmia before tumor treatment.

MicroRNA-Related Strategies to Improve Cardiac Function in Heart Failure.

Heart failure (HF) describes a group of manifestations caused by the failure of heart function as a pump that supports blood flow through the body. MicroRNAs (miRNAs), as one type of non-coding RNA molecule, have crucial roles in the etiology of HF. Accordingly, miRNAs related to HF may represent potential novel therapeutic targets. In this review, we first discuss the different roles of miRNAs in the development and diseases of the heart. We then outline commonly used miRNA chemical modifications and delivery systems. Further, we summarize the opportunities and challenges for HF-related miRNA therapeutics targets, and discuss the first clinical trial of an antisense drug (CDR132L) in patients with HF. Finally, we outline current and future challenges and potential new directions for miRNA-based therapeutics for HF.

MicroRNA-338-5p alleviates neuronal apoptosis via directly targeting BCL2L11 in APP/PS1 mice.

MicroRNAs have become pivotal modulators in the pathogenesis of Alzheimer's disease. MiR-338-5p is associated with neuronal differentiation and neurogenesis, and expressed aberrantly in patients with cognitive dysfunction. However, its role and potential mechanism involved in Alzheimer's disease remain to be elucidated. Herein, we showed that the expression of miR-338-5p decreased in APP/PS1 mice, accompanied by the elevation in the expression level of amyloid ß, which indicated a reverse relationship between Alzheimer's disease progression and miR-338-5p. In addition, lentiviral overexpression of miR-338-5p through intrahippocampal injection mitigated the amyloid plaque deposition and cognitive dysfunction in APP/PS1 mice, suggesting a protecting role of miR-338-5p against the development of Alzheimer's disease. Moreover, miR-338-5p decelerated apoptotic loss of neurons in APP/PS1 mice. MiR-338-5p decreased neuronal apoptosis in vitro induced by amyloid ß accumulation, which was attributed to the negative regulation of BCL2L11 by miR-338-5p, since the restoration of BCL2L11 eliminated the protective role of miR-338-5p against neuronal apoptosis. Taken together, all of these results may indicate miR-338-5p as an innovative modulator in the pathogenesis of Alzheimer's disease, and also suggest that the protective effect of miR-338-5p on neuronal apoptosis may underlie its beneficial effect on APP/PS1 mice.

[Establishment of porcine model of prolonged cardiac arrest and cardiopulmonary resuscitation electrically induced by ventricular fibrillation].

OBJECTIVE: To investigate the optimal injury time point of cardiac arrest (CA) induced electrically, and establish a reproducible prolonged CA and cardiopulmonary resuscitation (CPR) model in pigs. METHODS: Forty healthy domestic male pigs were randomly divided into four groups, which were ventricular fibrillation (VF) 8, 10, 11, and 12 minutes groups, each group for 10 animals. In these groups, VF was induced by alternating current delivered to right ventricular endocardium and untreated for 8, 10, 11, and 12 minutes, respectively, followed by 6 minutes of CPR procedure. The resuscitation and survival outcomes were recorded. Hemodynamic parameters and arterial blood gases of animals after successful resuscitation were measured and recorded for 6 hours. Those successful resuscitation animals were regularly evaluated for the neurological deficit score (NDS) and survival outcomes every 24 hours till 96 hours after resuscitation. RESULTS: The shortest duration of CPR (minute: 6.9±1.3) and the highest successful ratio of the first defibrillation (7/10) were observed in group VF 8 minutes, and the ratio of successful resuscitation was 100%. The best coronary perfusion pressure (CPP) during the CPR, less neurological impairment, longer survival time, more stable hemodynamics, and shorter time for arterial pH and lactate level restoring to the original state after CPR were also observed in group VF 8 minutes, and no severe damage was found in those animals. The longest duration of CPR (minute: 10.3±2.9) and the lowest successful ratio of the first defibrillation (1/10) were observed in group VF 12 minutes, and only 4 animals achieved restoration of spontaneous circulation (ROSC), and no animal survived to CPR 96 hours. The worst CPP during CPR and the highest NDS after resuscitation were also found in VF 12 minutes animals compared to those animals in the other groups. The injuries caused by ischemia and hypoxia in groups VF 10 minutes and VF 11 minutes were in between those of the groups VF 8 minutes and VF 12 minutes, and the duration of CPR were (7.0±2.1) minutes and (8.2±2.6) minutes. There were 9 and 7 animals achieved ROSC in groups VF 10 minutes and VF 11 minutes correspondingly, and 6 and 4 animals survived to 96 hours respectively. Obviously unstable hemodynamics was observed during the period of CPR 2 hours in the two groups. At CPR 1 hour, the heart rates (HR, beats/min) in groups VF 10 minutes and VF 11 minutes increased to 172 (155, 201) and 168 (136, 196) respectively, and the mean arterial pressures (MAP, mmHg, 1 mmHg = 0.133 kPa) declined to 97 (92, 100) and 81 (77, 100), the cardiac output (CO, L/min) decreased to 5.0 (4.0, 5.8), 3.7 (3.0, 5.4) correspondingly. Distinct injuries were found in the two groups [CPR 24-96 hours NDS in groups VF 10 minutes and VF 11 minutes: 180 (110, 255)-20 (0, 400) and 275 (223, 350)-240 (110, 400)], and the arterial pH of the two group decreased to 7.26±0.09 and 7.23±0.09 respectively, and the level of lactate (mmol/L) increased to 9.17±1.48 and 12.80±2.71 correspondingly at CPR 0.5 hour. Significantly lower pH was observed in group VF 11 minutes compared to group VF 8 minutes at CPR 0.5 hour (7.23±0.09 vs. 7.33±0.04, P < 0.05). The highest level of lactate (mmol/L) was also found at the same time point in group VF 11 minutes, which recovered to normal slowly, and was still significantly higher than groups VF 8, 10, 12 minutes (7.58±3.99 vs. 2.55±1.53, 2.13±2.00, 3.40±2.30, all P < 0.05) at CPR 4 hours. CONCLUSIONS: The longer duration of CA was, the more severe damage would be, the longer CPR time would be required, and the harder of the animals to achieve ROSC. In this prolonged CA and CPR porcine model, 10-11 minutes for untreated VF, was an optimal time point with appropriate successful rate of resuscitation, survival outcomes, and post-resuscitation injuries. Therefore, we recommended 10-11 minutes might be the rational length of no-flow time in this model.