Multimodal ultrasound diagnosis of epididymo-orchitis with secondary testicular infarction: A case report.

We report a case of a 48-year-old man with testicular infarction caused by epididymo-orchitis (EO). Multimodal ultrasound showed extensive necrosis of the testis, and the patient underwent right orchiectomy. Postoperative pathology confirmed extensive necrosis of the testis. After 3 months of follow-up, the examination of scrotal ultrasound showed that the left testis and epididymis had no obvious abnormality.

SEP-363856 exerts neuroprotection through the PI3K/AKT/GSK-3ß signaling pathway in a dual-hit neurodevelopmental model of schizophrenia-like mice.

Schizophrenia (SZ) is a serious, destructive neurodevelopmental disorder. Antipsychotic medications are the primary therapy approach for this illness, but it's important to pay attention to the adverse effects as well. Clinical studies for SZ are currently in phase ΙΙΙ for SEP-363856 (SEP-856)-a new antipsychotic that doesn't work on dopamine D2 receptors. However, the underlying action mechanism of SEP-856 remains unknown. This study aimed to evaluate the impact and underlying mechanisms of SEP-856 on SZ-like behavior in a perinatal MK-801 treatment combined with social isolation from the weaning to adulthood model (MK-SI). First, we created an animal model that resembles SZ that combines the perinatal MK-801 with social isolation from weaning to adulthood. Then, different classical behavioral tests were used to evaluate the antipsychotic properties of SEP-856. The levels of proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, and interleukin-1ß), apoptosis-related genes (Bax and Bcl-2), and synaptic plasticity-related genes (brain-derived neurotrophic factor [BDNF] and PSD-95) in the hippocampus were analyzed by quantitative real-time PCR. Hematoxylin and eosin staining were used to observe the morphology of neurons in the hippocampal DG subregions. Western blot was performed to detect the protein expression levels of BDNF, PSD-95, Bax, Bcl-2, PI3K, p-PI3K, AKT, p-AKT, GSK-3ß, p-GSK-3ß in the hippocampus. MK-SI neurodevelopmental disease model studies have shown that compared with sham group, MK-SI group exhibit higher levels of autonomic activity, stereotyped behaviors, withdrawal from social interactions, dysregulated sensorimotor gating, and impaired recognition and spatial memory. These findings imply that the MK-SI model can mimic symptoms similar to those of SZ. Compared with the MK-SI model, high doses of SEP-856 all significantly reduced increased activity, improved social interaction, reduced stereotyping behavior, reversed sensorimotor gating dysregulation, and improved recognition memory and spatial memory impairment in MK-SI mice. In addition, SEP-856 can reduce the release of proinflammatory factors in the MK-SI model, promote the expression of BDNF and PSD-95 in the hippocampus, correct the Bax/Bcl-2 imbalance, turn on the PI3K/AKT/GSK-3ß signaling pathway, and ultimately help the MK-SI mice's behavioral abnormalities. SEP-856 may play an antipsychotic role in MK-SI "dual-hit" model-induced SZ-like behavior mice by promoting synaptic plasticity recovery, decreasing death of hippocampal neurons, lowering the production of pro-inflammatory substances in the hippocampal region, and subsequently initiating the PI3K/AKT/GSK-3ß signaling cascade.

Left atrial dysfunction can independently predict exercise capacity in patients with chronic heart failure who use beta-blockers.

BACKGROUND: Beta-blockers are first-line clinical drugs for the treatment of chronic heart failure (CHF). In the guidelines for cardiac rehabilitation, patients with heart failure who do or do not receive beta-blocker therapy have different reference thresholds for maximal oxygen uptake (VO2max). It has been reported that left atrial (LA) strain can be used to predict VO2max in patients with heart failure, which can be used to assess exercise capacity. However, most existing studies included patients who did not receive beta-blocker therapy, which could have a heterogeneous influence on the conclusions. For the vast majority of CHF patients receiving beta-blockers, the exact relationship between LA strain parameters and exercise capacity is unclear. METHODS: This cross-sectional study enrolled 73 patients with CHF who received beta-blockers. All patients underwent a thorough resting echocardiogram and a cardiopulmonary exercise test to obtain VO2max, which was used to reflect exercise capacity. RESULTS: LA reservoir strain, LA maximum volume index (LAVImax), LA minimum volume index (LAVImin) (P < 0.0001) and LA booster strain (P < 0.01) were all significantly correlated with VO2max, and LA conduit strain was significantly correlated with VO2max (P < 0.05) after adjusting for sex, age, and body mass index. LA reservoir strain, LAVImax, LAVImin (P < 0.001), and LA booster strain (P < 0.05) were significantly correlated with VO2max after adjusting for left ventricular ejection fraction, the ratio of transmitral E velocity to tissue Doppler mitral annulus e' velocity (E/e'), and tricuspid annular plane systolic excursion. LA reservoir strain with a cutoff value of 24.9% had a sensitivity of 74% and specificity of 63% for the identification of patients with VO2max < 16 mL/kg/min. CONCLUSION: Among CHF patients receiving beta-blocker therapy, resting LA strain is linearly correlated with exercise capacity. LA reservoir strain is a robust independent predictor of reduced exercise capacity among all resting echocardiography parameters. CLINICAL TRIAL REGISTRATION: This study is a part of the Baduanjin-Eight-Silken-Movement with Self-efficacy Building for Patients with Chronic Heart Failure (BESMILE-HF) trial NCT03180320 (ClinicalTrials.gov, registration date: 08/06/2017).

Incremental value of combinatorial contrast echocardiography and 18F-fluorodeoxyglucose positron emission tomography/computed tomography in giant right atrial myxomas.

Although several studies have shown that myocardial contrast echocardiography and 18-FDG PET/CT can differentiate between benign and malignant intracardiac masses, it is rarely used in practice to evaluate myxoma. This case describes the contrast echocardiography and 18-FDG PET/CT findings of a giant myxoma with an atypical location and subclinical symptoms.

Non-Histone Lysine Crotonylation Is Involved in the Regulation of White Fat Browning.

Lysine crotonylation modification is a novel acylation modification that is similar to acetylation modification. Studies have found that protein acetylation plays an important regulatory part in the occurrence and prevention of obesity and is involved in the regulation of glucose metabolism, tricarboxylic acid cycle, white fat browning and fatty acid metabolism. Therefore, we speculate that protein crotonylation may also play a more vital role in regulating the browning of white fat. To verify this conjecture, we identified 7254 crotonyl modification sites and 1629 modified proteins in iWAT of white fat browning model mice by affinity enrichment and liquid chromatography-mass spectrometry (LC-MS/MS). We selected five representative proteins in the metabolic process, namely glycerol-3-phosphate dehydrogenase 1 (GPD1), fatty acid binding protein 4 (FABP4), adenylate kinase 2 (AK2), triosephosphate isomerase 1 (TPI1) and NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 8 (NDUFA8). Through qPCR, Western blotting, immunofluorescence staining, Oil Red O staining and HE staining, we demonstrated that GPD1 and FABP4 inhibited white fat browning, while AK2, TPI1 and NDUFA8 promoted white fat browning. GPD1 and FABP4 proteins were downregulated by crotonylation modification, while AK2, TPI1 and NDUFA8 proteins were upregulated by crotonylation modification. Further detection found that the crotonylation modification of GPD1, FABP4, AK2, TPI1 and NDUFA8 promoted white fat browning, which was consistent with the sequencing results. These results indicate that the protein crotonylation is involved in regulating white fat browning, which is of great significance for controlling obesity and treating obesity-related diseases.

Collagen XV Promotes ER Stress-Induced Inflammation through Activating Integrin ß1/FAK Signaling Pathway and M1 Macrophage Polarization in Adipose Tissue.

Collagen XV (Col XV), a basement membrane (BM) component, is highly expressed in adipose tissue, and studies have found that Col XV is related to extracellular matrix (ECM) remodeling involving in adipose tissue fibrosis and inflammation. Furthermore, the ECM is essential for maintaining normal development and tissue function. In this study, we found that Col XV is related to the endoplasmic reticulum stress (ERS) and inflammation of adipose tissue. Moreover, we found that overexpression of Col XV in mice could cause macrophages to infiltrate white adipose tissue (iWAT). At the same time, the expression of the ERS sensor IRE1α (Inositol-Requiring Enzyme-1α) was significantly up-regulated, which intensified the inflammation of adipose tissue and the polarization of M1 macrophages after the overexpression of Col XV in mice. In addition, after overexpression of Col XV, the intracellular Ca2+ concentration was significantly increased. Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1α, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78). After treatment with IRE1α inhibitor STF-083010, the results showed that the expression of adipocyte inflammation-related genes interleukin 6 (IL-6) and tumor necrosis factor α (TNFα) significantly were decreased. Our results demonstrate that Col XV induces ER-stress in adipocytes by activating the Integrinß1/FAK pathway and disrupting the intracellular Ca2+ balance. At the same time, Col XV regulates the inflammation induced by ER stress in adipocytes by promoting IRE1α/XBP1 (X-Box binding protein 1) signaling. Our study provides new ideas for solving the problems of adipose tissue metabolism disorders caused by abnormal accumulation of ECM.

The Mechanism of Leptin on Inhibiting Fibrosis and Promoting Browning of White Fat by Reducing ITGA5 in Mice.

Leptin is a small molecule protein secreted by adipocytes, which can promote white fat browning through activating the hypothalamic nervous system and inhibiting downstream signaling pathways. Moreover, white fat browning has been proven to alleviate fat tissue fibrosis. This study explores the mechanism of leptin in regulating adipose tissue fibrosis and white fat browning. After treating mice with leptin, we screened out the recombinant integrin alpha 5 (ITGA5) through proteomics sequencing, which may play a role in adipose tissue fibrosis. Through real-time quantitative PCR (qPCR), western blotting (WB), hematoxylin-eosin (HE) staining, Masson's trichrome, immunofluorescence, immunohistochemistry, etc., the results showed that after leptin treated adipocytes, the expression of fibrosis-related genes and ITGA5 was significantly down-regulated in adipocytes. We constructed fibrosis model through transforming growth factor-ß (TGF-ß) and a high-fat diet (HFD), and treated with ITGA5 overexpression vector and interference fragments. The results indicated the expression of fibrosis-related genes were significantly down-regulated after interfering with ITGA5. After treating adipocytes with wortmannin, fibrosis-related gene expression was inhibited after overexpression of ITGA5. Moreover, after injecting mice with leptin, we also found that leptin significantly up-regulated the expression of adipose tissue browning-related genes. Overall, our research shows that leptin can inhibit the activation of phosphatidylinositol 3 kinase (PI3K)-protein kinase B (AKT) signaling pathway by reducing the expression of ITGA5, which could alleviate adipose tissue fibrosis, and further promote white fat browning. Our research provides a theoretical basis for further research on the effect of leptin in fibrosis-related adipose tissue metabolism.

miR-34a/c induce caprine endometrial epithelial cell apoptosis by regulating circ-8073/CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways.

microRNAs (miRNAs) and circular RNAs (circRNAs) are important for endometrial receptivity establishment and embryo implantation in mammals. miR-34a and miR-34c are highly expressed in caprine receptive endometrium (RE). Herein, the functions and mechanisms of miR-34a/c in caprine endometrial epithelial cell (CEEC) apoptosis and RE establishment were investigated. miR-34a/c downregulated the expression level of centrosomal protein 55 (CEP55) and were sponged by circRNA8073 (circ-8073), thereby exhibiting a negative interaction in CEEC. miR-34a/c induced CEEC apoptosis by targeting circ-8073/CEP55 through the regulation of the RAS/RAF/MEK/ERK and phosphoitide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways. Positive and negative feedback loops and cross-talk were documented between the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways. miR-34a/c regulated the levels of RE marker genes, including forkhead box M1, vascular endothelial growth factor, and osteopontin (OPN). These results suggest that miR-34a/c not only induce CEEC apoptosis by binding to circ-8073 and CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways, but may also regulate RE establishment in dairy goats.

Circ-8073 regulates CEP55 by sponging miR-449a to promote caprine endometrial epithelial cells proliferation via the PI3K/AKT/mTOR pathway.

Circular RNAs (circRNAs) are a large class of endogenous non-coding RNAs that function as regulators in various cells and tissues. Here, the function and mechanism of circRNA8073 (Circ-8073) on endometrial epithelial cells (EECs) and the development of endometrial receptivity were investigated in dairy goats. Circ-8073 could bind to and inhibit miR-449a activity. Circ-8073 binding to the target site of miR-449a had a negative feedback relationship. Centrosomal protein55 (CEP55) was a direct target gene of miR-449a, and Circ-8073 could increase the expression levels of CEP55 by sponging miR-449a in EECs in vitro. Circ-8073/miR-449a/CEP55 could promote EECs proliferation via the PI3K/AKT/mTOR pathway. In addition, CEP55 could regulate the expression levels of vascular endothelial growth factor (VEGF) and forkhead box M1 (FOXM1) in EECs, which contributed to the development of endometrial receptivity. These findings showed that Circ-8073 regulated CEP55 by sponging miR-449a to promote EEC proliferation via the PI3K/AKT/mTOR pathway, suggesting that it could function as a regulator in the development of endometrial receptivity in dairy goats.

LncRNA882 regulates leukemia inhibitory factor (LIF) by sponging miR-15b in the endometrial epithelium cells of dairy goat.

Despite the fact that long noncoding RNAs (lncRNAs) play roles in almost all biological processes, little is known about their biological function in the endometrium during the formation of endometrial receptivity. In this study, a comprehensive analysis of lncRNAs in goat endometrial tissues on Day 5 (prereceptive endometrium, PE) and Day 15 (receptive endometrium, RE) of pregnancy was performed by using RNA-Seq. As a result, 668 differentially expressed lncRNAs (DELs) were found between the PE and RE. Further study showed that lncRNA882, regulated by estrogen (E2) and progestin (P4), could act as competing endogenous RNAs (ceRNAs) for miR-15b, which inhibited the expression of transforming growth factor-b-activated kinase 1 binding protein 3 (TAB3) and then indirectly regulated the level of leukemia inhibitory factor (LIF). This was helpful for the formation of endometrial receptivity in dairy goats. In conclusion, we elucidated the endometrium lncRNA profiles of PE and RE in dairy goats; lncRNA882 acted as a ceRNA for miR-15b and then indirectly regulated the level of LIF in goat endometrial epithelium cells. Thus, this study helped us to better understand the molecular regulation of endometrial receptivity in dairy goats.

Ultra-broadband infrared metasurface absorber: reply.

This is a reply to the comment "Ultra-broadband infrared metasurface absorber: comment."

Testin was regulated by circRNA3175-miR182 and inhibited endometrial epithelial cell apoptosis in pre-receptive endometrium of dairy goats.

Circular RNAs (circRNAs) in various tissues and cell types from mammalian sources have been studied. However, present knowledge on circRNAs in the development of pre-receptive endometrium (PE) in dairy goats is limited. In the pre-receptive endometrium of dairy goats, higher circRNA3175 (ciR3175) levels, lower miR-182 levels and higher Testin (TES) levels were detected. And ciR3175 could decreased the miR-182 levels by acting as a miRNA sponge, and miR-182 could down-regulated the expression level of TES via the predicted target site in endometrial epithelial cells (EECs) in vitro. Via this way, ciR3175 functioned as a competing endogenous RNAs (ceRNA) that sequestered miR-182, thereby protecting TES transcripts from miR-182-mediated suppression in EECs in vitro. Further, TES inhibited EECs apoptosis by decreasing the expression level of BCL-2/BAX via the MAPK pathway. Thus, a ciR3175-miR182-TES pathway in the endometrium was identified in EECs, and the modulation of which could emerge as a potential target in regulating the pre-receptive endometrium development in dairy goats.

CircRNA-9119 regulates the expression of prostaglandin-endoperoxide synthase 2 (PTGS2) by sponging miR-26a in the endometrial epithelial cells of dairy goat.

Circular RNAs (circRNAs) have been found to play important functional roles in epigenetic regulation under certain physiological and pathological conditions. However, knowledge of circRNAs during the development of receptive endometrium (RE) from pre-RE is limited. In the RE of dairy goats, higher circRNA-9119 levels, with lower miR-26a and higher prostaglandin-endoperoxide synthase 2 (PTGS2) levels, were detected. Further study showed that circRNA-9119 decreased levels of miR-26a by acting as a microRNA sponge, and that miR-26a downregulated the expression of PTGS2 via the predicted target site in endometrial epithelial cells (EECs) of dairy goats in vitro. In this way, circRNA-9119 functioned as a competing endogenous RNAs (ceRNA) that sequestered miR-26a, thereby protecting PTGS2 transcripts from miR-26a-mediated suppression in dairy goat EECs in vitro. Furthermore, PTGS2 participated in the regulation of some protein markers for endometrial receptivity in dairy goat EECs in vitro. Thus, a circRNA-9119-miR-26a-PTGS2 pathway in the endometrium was identified, and modulation of circRNA-9119-miR-26a-PTGS2 expression in EECs may emerge as a potential target to regulate the development of RE.

Ultra-broadband infrared metasurface absorber.

By using sub-wavelength resonators, metamaterial absorber shows great potential in many scientific and technical applications due to its perfect absorption characteristics. For most practical applications, the absorption bandwidth is one of the most important performance metrics. In this paper, we demonstrate the design of an ultra-broadband infrared absorber based on metasurface. Compared with the prior work [Opt. Express22(S7), A1713-A1724 (2014)], the proposed absorber shows more than twice the absorption bandwidth. The simulated total absorption exceeds 90% from 7.8 to 12.1 um and the full width at half maximum is 50% (from 7.5 to 12.5 µm), which is achieved by using a single layer of metasurface. Further study demonstrates that the absorption bandwidth can be greatly expanded by using two layers of metasurface, i.e. dual-layered absorber. The total absorption of the dual-layered absorber exceeds 80% from 5.2 to 13.7 um and the full width at half maximum is 95% (from 5.1 to 14.1 µm), much greater than those previously reported for infrared spectrum. The absorption decreases with fluctuations as the incident angle increases but remains quasi-constant up to relatively large angles.

Dihydrolipoyl dehydrogenase promotes white adipocytes browning by activating the RAS/ERK pathway and undergoing crotonylation modification.

Acetylation modification has a wide range of functional roles in almost all physiological processes, such as transcription and energy metabolism. Crotonylation modification is mainly involved in RNA processing, nucleic acid metabolism, chromosome assembly and gene expression, and it's found that there is a competitive relationship between crotonylation modification and acetylation modification. Previous study found that dihydrolipoyl dehydrogenase (DLD) was highly expressed in brown adipose tissue (BAT) of white adipose tissue browning model mice, suggesting that DLD is closely related to white fat browning. This study was performed by quantitative real-time PCR (qPCR), Western blotting (WB), Enzyme-linked immunosorbent assay (ELISA), Immunofluorescence staining, JC-1 staining, Mito-Tracker Red CMXRos staining, Oil red O staining, Bodipy staining, HE staining, and Blood lipid quadruple test. The assay revealed that DLD promotes browning of white adipose tissue in mice. Cellularly, DLD was found to promote white adipocytes browning by activating mitochondrial function through the RAS/ERK pathway. Further studies revealed that the crotonylation modification and acetylation modification of DLD had mutual inhibitory effects. Meanwhile, DLD crotonylation promoted white adipocytes browning, while DLD acetylation did the opposite. Finally, protein interaction analysis and Co-immunoprecipitation (Co-IP) assays identified Sirtuin3 (SIRT3) as a decrotonylation and deacetylation modification enzyme of regulates DLD. In conclusion, DLD promotes browning of white adipocytes by activating mitochondrial function through crotonylation modification and the RAS/ERK pathway, providing a theoretical basis for the control and treatment of obesity, which is of great significance for the treatment of obesity and obesity-related diseases in the future.

NDUFA9 and its crotonylation modification promote browning of white adipocytes by activating mitochondrial function in mice.

Protein crotonylation plays a role in regulating cellular metabolism, gene expression, and other biological processes. NDUFA9 (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 9) is closely associated with the activity and function of mitochondrial respiratory chain complex I. Mitochondrial function and respiratory chain are closely related to browning of white adipocytes, it's speculated that NDUFA9 and its crotonylation are associated with browning of white adipocytes. Firstly, the effect of NDUFA9 on white adipose tissue was verified in white fat browning model mice, and it was found that NDUFA9 promoted mitochondrial respiration, thermogenesis, and browning of white adipose tissue. Secondly, in cellular studies, it was discovered that NDUFA9 facilitated browning of white adipocytes by enhancing mitochondrial function, mitochondrial complex I activity, ATP synthesis, and mitochondrial respiration. Again, the level of NDUFA9 crotonylation was increased by treating cells with vorinostat (SAHA)+sodium crotonate (NaCr) and overexpressing NDUFA9, it was found that NDUFA9 crotonylation promoted browning of white adipocytes. Meanwhile, the acetylation level of NDUFA9 was increased by treating cells with SAHA+sodium acetate (NaAc) and overexpressing NDUFA9, the assay revealed that NDUFA9 acetylation inhibited white adipocytes browning. Finally, combined with the competitive relationship between acetylation and crotonylation, it was also demonstrated that NDUFA9 crotonylation promoted browning of white adipocytes. Above results indicate that NDUFA9 and its crotonylation modification promote mitochondrial function, which in turn promotes browning of white adipocytes. This study establishes a theoretical foundation for the management and intervention of obesity, which is crucial in addressing obesity and related medical conditions in the future.

ILC2s control obesity by regulating energy homeostasis and browning of white fat.

Innate lymphoid cells (ILCs) have been a hot topic in recent research, they are widely distributed in vivo and play an important role in different tissues. The important role of group 2 innate lymphoid cells (ILC2s) in the conversion of white fat into beige fat has attracted widespread attention. Studies have shown that ILC2s regulate adipocyte differentiation and lipid metabolism. This article reviews the types and functions of ILCs, focusing on the relationship between differentiation, development and function of ILC2s, and elaborates on the relationship between peripheral ILC2s and browning of white fat and body energy homeostasis. This has important implications for the future treatment of obesity and related metabolic diseases.

Construction of an aging-related risk signature in high-grade serous ovarian cancer for predicting survival outcome and immunogenicity.

Studies have shown that aging significantly impacts tumorigenesis, survival outcome, and treatment efficacy in various tumors, covering high-grade serous ovarian cancer (HGSOC). Therefore, the objective for this investigation is to construct an aging-relevant risk signature for the first time, which will help evaluate the immunogenicity and survival status for patients with HGSOC. Totaling 1727 patients with HGSOC, along with their mRNA genomic data and clinical survival data, were obtained based on 5 independent cohorts. The Lasso-Cox regression model was utilized to identify the aging genes that had the most significant impact on prognosis. The risk signature was developed by integrating the determined gene expression and accordant model weights. Additionally, immunocytes in the microenvironment, signaling pathways, and immune-relevant signatures were assessed based on distinct risk subgroups. Finally, 2 cohorts that underwent treatment with immune checkpoint inhibitor (ICI) were employed to confirm the effects of identified risk signature on ICI efficacy. An aging signature was constructed from 12 relevant genes, which showed improved survival outcomes in low-risk HGSOC patients across discovery and 4 validation cohorts (all P < .05). The low-risk subgroup showed better immunocyte infiltration and higher enrichment of immune pathways and ICI predictors based on further immunology analysis. Notably, in the immunotherapeutic cohorts, low-risk aging signature was observed to link to better immunotherapeutic outcomes and increased response rates. Together, our constructed signature of aging has the potential to assess not only the prognosis outcome and immunogenicity, but also, importantly, the efficacy of ICI treatment. This signature provides valuable insights for prognosis prediction and immunotherapeutic effect evaluation, ultimately promoting individualized treatment for HGSOC patients.

Case report: multi-modality imaging of a right ventricular fibroma in a teenager.

Background: Cardiac fibroma is a rare primary benign tumour of the heart. It often causes arrhythmia, endangers the lives of patients, and has a worse prognosis than other benign tumours. We report a 14-year-old female patient with a right ventricular fibroma. Various preoperative imaging examinations showed that the lesion was benign, and postoperative pathology confirmed that the lesions were fibroma. Case summary: A 14-year-old female patient visited her doctor for more than 5 months because of a heart murmur. Echocardiography revealed a slightly hyperechoic mass in the right ventricle, and on myocardial perfusion contrast imaging, the lesion showed equal enhancement. And the lesion also showed enhancement on contrast-enhanced gated cardiac computed tomography (CT). Contrast-enhanced magnetic resonance imaging (MRI) of the heart revealed that the lesion was isointense on T1-weighted image (T1WI), and isointense to slightly hyperintense on T2-weighted image (T2WI). The lesion was significantly homogeneously enhanced on a delayed enhancement scan. A positron emission tomography-CT (PET-CT) with 18F-fluorodeoxyglucose (18F-FDG) demonstrated that the mass showed lower levels of 18F-FDG uptake. These features suggested this lesion was a benign lesion. The postoperative pathology suggested the lesion was a right ventricular fibroma. The patient was discharged 14 days after surgery and remains disease-free and asymptomatic 14 months after surgery. Discussion: Cardiac fibromas are histologically benign, but they can cause obstruction and malignant arrhythmia. The gold standard for diagnosing fibroma is pathology. However, in the absence of pathology, it is necessary to use various imaging methods to evaluate the lesions to distinguish between benign and malignant tumours.

Leptin: an entry point for the treatment of peripheral tissue fibrosis and related diseases.

Leptin is a small peptide mainly secreted by adipocyte, which acts on the central nervous system of the hypothalamus to regulate the body's energy balance by inhibiting food intake, it also can directly act on specific cells through leptin receptors (for example, ObRa, which exists in the blood-brain barrier or kidneys), thereby affect cell metabolism. Excessive deposition of extracellular matrix (ECM) causes damage to normal tissues or destruction of organ structure, which will eventually lead to tissue or organ fibrosis. The sustainable development of fibrosis can lead to structural damage and functional decline of organs, and even exhaustion, which seriously threatens human health and life. In recent years, studies have found that leptin directly alleviates the fibrosis process of various tissues and organs in mammals. Therefore, we speculate that leptin may become a significant treatment for fibrosis of various tissues and organs in the future. So, the main purpose of this review is to explore the specific mechanism of leptin in the process of fibrosis in multiple tissues and organs, and to provide a theoretical basis for the treatment of various tissues and organs fibrosis and related diseases caused by it, which is of great significance in the future.