A rare inflammatory myofibroblastic tumor appearing both inside and outside the heart.

BACKGROUND: Inflammatory myofibroblastic tumor (IMT) is an uncommon cardiac tumor that primarily affects infants, children, and young adults. While complete surgical resection generally leads to a favorable prognosis, accurate diagnostic tests remain limited. CASE PRESENTATION: We describe the case of a 26-year-old female who had a dual tumor inside and outside the heart and was misdiagnosed by echocardiography and MRI. We also review 71 cases of cardiac IMTs from the literature regarding their epidemiology, clinical presentation, and outcome. CONCLUSION: Early detection of this rare disorder is essential for optimal surgical management.

FOXO3-Activated circFGFBP1 Inhibits Extracellular Matrix Degradation and Nucleus Pulposus Cell Death via miR-9-5p/BMP2 Axis in Intervertebral Disc Degeneration In Vivo and In Vitro.

(1) Background: intervertebral disc degeneration (IVDD) defined as the degenerative changes in intervertebral disc is characterized by extracellular matrix (ECM) degradation and death in nucleus pulposus (NP) cells. (2) Methods: The model of IVDD was established in male Sprague Dawley rats using a puncture of a 21-gauge needle at the endplates located in the L4/5 intervertebral disc. Primary NP cells were stimulated by 10 ng/mL IL-1ß for 24 h to mimic IVDD impairment in vitro. (3) Results: circFGFBP1 was downregulated in the IVDD samples. circFGFBP1 upregulation inhibited apoptosis and extracellular matrix (ECM) degradation and promoted proliferation in IL-1ß-stimulated NP cells. Additionally, circFGFBP1 upregulation mitigated the loss of NP tissue and the destruction of the intervertebral disc structure in vivo during IVDD. FOXO3 could bind to the circFGFBP1 promoter to enhance its expression. circFGFBP1 upregulated BMP2 expression in NP via sponging miR-9-5p. FOXO3 enhanced the protection of circFGFBP1 in IL-1ß-stimulated NP cells, whereas a miR-9-5p increase partly reversed the protection. miR-9-5p downregulation contributed to the survival of IL-1ß-stimulated NP cells, which was partially reversed by BMP2 silence. (4) Conclusions: FOXO3 could activate the transcription of circFGFBP1 via binding to its promoter, which resulted in the enhancement of BMP2 via sponging miR-9-5p and then inhibited apoptosis and ECM degradation in NP cells during IVDD.

Exosomal miR-103-3p from LPS-activated THP-1 macrophage contributes to the activation of hepatic stellate cells.

Hepatic fibrosis occurs during chronic hepatic injury and is involved in hepatic stellate cells (HSCs) activated by several types of immune cells. Among the immune cells, hepatic macrophages and their crosstalk with HSCs play a vital role in all stages of hepatic fibrosis. Exosomes, which are 30-150 nm lipid bilayer vehicles, can transfer specific lipid, nucleic acids, proteins, and other bioactive molecules. Exosomes can act as good communication between macrophages and HSCs. Herein, we investigated the role of exosomes between THP-1 macrophage and HSCs in the progression of liver fibrosis. Exosomes originating from lipopolysaccharide (LPS)-treated THP-1 macrophages promoted HSCs proliferation and induced the increased expression of fibrotic genes. LPS could alter the miRNA profile in exosomes secreted from THP-1 macrophages. The changed miR-103-3p in exosomes could promote HSCs proliferation and activation by targeting Krüppel-like factor 4 (KLF4) and it plays important roles in the crosstalk between THP-1 macrophages and HSCs during the progression of liver fibrosis. Moreover, miR-103-3p in serum exosomes from liver fibrosis patients could be a biomarker for liver fibrosis. Therefore, exosomes may have important roles in the crosstalk between macrophage and HSCs in the progression of chronic liver diseases.

Kinetic magnetic resonance imaging analysis of thoracolumbar segmental mobility in patients without significant spondylosis.

To observe thoracolumbar segmental mobility using kinetic magnetic resonance imaging (kMRI) in patients with minimal thoracolumbar spondylosis and establish normal values for translational and angular segmental motion as well as the relative contribution of each segment to total thoracolumbar segmental motion in order to obtain a more complete understanding of this segmental motion in healthy and pathological conditions.Mid-sagittal images obtained by weight-bearing, multi-position kMRI in patients with symptomatic low back pain or radiculopathy were reviewed. The translational motion and angular variation of each segment from T10-L2 were calculated using MRAnalyzer Automated software. Only patients with a Pfirrmann grade of I or II, indicating minimal disc disease, for all thoracolumbar discs from T10-T11 to L1-L2 were included for further analysis.The mean translational motion measurements for each level of the lumbar spine were 1.15 mm at T10-T11, 1.20 mm at T11-T12, 1.23 mm at T12-L1, and 1.34 mm at L1-L2 (P < .05 for L1-L2 vs T10-T11). The mean angular motion measurements at each level were 3.26° at T10-T11, 3.92° at T11-T12, 4.95° at T12-L1, and 6.85° at L1-L2. The L1-L2 segment had significantly more angular motion than all other levels (P < .05). The mean percentage contribution of each level to the total angular mobility of the thoracolumbar spine was highest at L1-L2 (36.1%) and least at T10-T11 (17.1%; P < .01).Segmental motion was greatest in the proximal lumbar levels, and angular motion showed a gradually increasing trend from T10 to L2.

Bone morphogenetic protein 2 alleviated intervertebral disc degeneration through mediating the degradation of ECM and apoptosis of nucleus pulposus cells via the PI3K/Akt pathway.

The present study aimed to explore the underlying mechanisms of bone morphogenetic protein 2 (BMP2) in alleviating intervertebral disc degeneration (IDD). A rat puncture IDD model was constructed, and the rats were randomly divided into six groups: Control; IDD (model); IDD+PBS [containing 1010 adeno­associated virus serotype 2 (AAV)]; and IDD + AAV2­BMP2 (106, 108 and 1010). IL­1ß was used to treat primary nucleus pulposus (NP) cells to mimic IDD in vitro. The effects of BMP2 in IDD were determined by magnetic resonance imaging (MRI), hematoxylin and eosin staining and Alcian Blue staining in vivo. The levels of collagen II, aggrecan, transcription factor SOX9 (SOX9) and matrix metalloproteinase 13 (MMP­13) were examined using western blot analysis and reverse transcription quantitative polymerase chain reaction (RT­qPCR) in NP tissues and cells. The expression of C­telopeptide of type II collagen (CTX­II) in the sera or cell supernatants was determined by ELISA. In addition, the levels of phosphorylation of phosphoinositide 3­kinase (PI3K) and protein kinase B (Akt), and the levels of apoptosis­associated proteins and apoptosis ratio of NP cells were also determined by western blot analysis and flow cytometry, respectively. LY29400, an inhibitor of PI3K, was used to additionally confirm the signal pathway mechanism of BMP2 treatment in IDD. BMP2 significantly extended the interval between discs and alleviated the fibrous ring rupture and the decrease in the levels of glycoproteins in IDD rats, as determined by MRI and histological staining. Additionally, BMP2 treatment significantly upregulated the levels of collagen II, aggrecan and SOX9, but downregulated the levels of MMP­13 and CTX­II in IDD rats and NP cells in a dose­dependent manner. Concurrently, recombinant human (rh)BMP2 pretreatment also significantly decreased the apoptosis ratio of interleukin (IL)­1ß­treated NP cells via downregulating the level of cleaved caspase­3 and upregulating the level of uncleaved poly (adenosine 5'­diphosphate­ribose) polymerase. It was demonstrated that rhBMP2 also significantly decreased the inflammatory response in NP tissues and cells, based on levels of IL­6, TNF­α and IL­10. In addition, rhBMP2 inhibited cell apoptosis via upregulating the phosphorylation levels of the PI3K/Akt signaling pathway, and LY29400 pretreatment inhibited the effects of BMP2 in IL­1ß treated NP cells. BMP2 alleviated IDD via the PI3K/Akt signaling pathway by inhibiting NP cell apoptosis and decreasing the levels of matrix proteins.