Case report: A case of primary cardiac malignant mesothelioma.

Primary cardiac malignant tumors are extremely rare, making up about 10% of all primary cardiac tumors. Most of these tumors are primary sarcomas, with primary mesothelioma being even less common. This report details a 53-year-old male patient diagnosed with primary cardiac malignant mesothelioma. The patient had symptoms of chest pain and difficulty breathing. A CT scan showed an enlarged heart, fluid around the heart, and irregular thickening of the pericardium. Diagnosis was confirmed through a surgical biopsy, which showed the presence of malignant mesothelioma. After the procedure, the patient received appropriate cardiac support. Although stable at discharge, the patient unfortunately died three months later due to severe wheezing. There may be a potential link between exposure to radioactive iodine treatment and this outcome. This case highlights the diagnostic and treatment challenges of primary cardiac malignant tumors and reminds physicians to consider this rare disease when evaluating patients with similar symptoms.

The role of RUNX1/NF-κB in regulating PVAT inflammation in aortic dissection.

The pathogenesis of aortic dissection (AD), an aortic disease associated with high mortality, involves significant vascular inflammatory infiltration. However, the precise relationship between perivascular adipose tissue (PVAT) and aortic dissection remains incompletely understood. The objective of this study is to investigate the role of PVAT inflammation in the pathogenesis of aortic dissection and identify novel therapeutic targets for this disease. The mouse model of aortic dissection was established in this study through intraperitoneal injection of Ang II and administration of BAPN in drinking water. Additionally, control groups were established at different time points including the 2-week group, 3-week group, and 4-week group. qPCR and immunohistochemistry techniques were employed to detect the expression of inflammatory markers and RUNX1 in PVAT surrounding the thoracic aorta in mice. Additionally, an aortic dissection model was established using RUNX1 knockout mice, and the aforementioned indicators were assessed. The 3T3-L1 cells were induced to differentiate into mature adipocytes in vitro, followed by lentivirus transfection for the knockdown or overexpression of RUNX1. The study aimed to investigate the potential cell-to-cell interactions by co-culturing 3T3-L1 cells with A7r5 or RAW264.7 cells. Subsequently, human aortic PVAT samples were obtained through clinical surgery and the aforementioned indicators were detected. In comparison to the control group, the aortic dissection model group exhibited decreased expression of MMP-2 and NF-κB in PVAT, while TNF-α and RUNX1 expression increased. Suppression of RUNX1 expression resulted in increased MMP-2 and NF-κB expression in PVAT, along with decreased TNF-α expression. Overexpression of RUNX1 upregulated the expression levels of NF-Κb, MMP-2, and TNF-α in adipocytes, whereas knockdown of RUNX1 exerted an opposite effect. Macrophages co-cultured with adipocytes overexpressing RUNX1 exhibited enhanced CD86 expression, while vascular smooth muscle cells co-cultured with these adipocytes showed reduced α-SMA expression. In human samples, there was an increase in both RUNX1 and MMP-2 expression levels, accompanied by a decrease in TNF-α and NF-Κb expression. The presence of aortic dissection is accompanied by evident inflammatory alterations in the PVAT, and this phenomenon appears to be associated with the involvement of RUNX1. It is plausible that the regulation of PVAT's inflammatory changes by RUNX1/NF-κB signaling pathway plays a role in the pathogenesis of aortic dissection.

An X-Band CMOS Digital Phased Array Radar from Hardware to Software.

Phased array technology features rapid and directional scanning and has become a promising approach for remote sensing and wireless communication. In addition, element-level digitization has increased the feasibility of complicated signal processing and simultaneous multi-beamforming processes. However, the high cost and bulky characteristics of beam-steering systems have prevented their extensive application. In this paper, an X-band element-level digital phased array radar utilizing fully integrated complementary metal-oxide-semiconductor (CMOS) transceivers is proposed for achieving a low-cost and compact-size digital beamforming system. An 8-10 GHz transceiver system-on-chip (SoC) fabricated in 65 nm CMOS technology offers baseband filtering, frequency translation, and global clock synchronization through the proposed periodic pulse injection technique. A 16-element subarray module with an SoC integration, antenna-in-package, and tile array configuration achieves digital beamforming, back-end computing, and dc-dc conversion with a size of 317 × 149 × 74.6 mm3. A radar demonstrator with scalable subarray modules simultaneously realizes range sensing and azimuth recognition for pulsed radar configurations. Captured by the suggested software-defined pulsed radar, a complete range-azimuth figure with a 1 km maximum observation range can be displayed within 150 ms under the current implementation.

Andrographolide inhibits NF-kappaBeta activation and attenuates neointimal hyperplasia in arterial restenosis.

The NF-kappaBeta transcription factors modulate the expression of tissue factor (TF), E-selectin (CD62E) and vascular cell adhesion molecule-1 (VCAM-1), which are essential for thrombosis and inflammation. We have previously shown that andrographolide (Andro) covalently modifies the reduced cysteine(62) of p50 - a major subunit of NF-kappaBeta transcription factors, thus blocking the binding of NF-kappaBeta transcription factors to the promoters of their target genes, preventing NF-kappaBeta activation and inhibiting inflammation in vitro and in vivo. Here we report that Andro, but not its inactive structural analog 4H-Andro, significantly suppressed the proliferation of arterial neointima ( approximately 60% reduction) in a murine model of arterial restenosis. Consistently, p50(-/-) mice manifested attenuated neointimal hyperplasia upon arterial ligation. Notably, the same dosage of Andro did not further reduce neointimal formation in p50(-/-) mice, which implicates the specificity of Andro on p50 for treating experimental arterial restenosis. The upregulation of NF-kappaBeta target genes, including TF, E-selectin and VCAM-1, and the increased deposition of leukocytes (mainly CD68+ macrophages) were clearly detected within the injured arterial walls, all of which were significantly abolished by treatment with Andro or genetic deletion of p50. The expression of TF, E-selectin and VCAM-1 was also markedly upregulated in the patient sample of thrombotic vasculitis, indicating the clinical relevance of NF-kappaBeta activation in the pathogeneses of occlusive arterial diseases. Our data thus indicate that, by the downregulation of the NF-kappaBeta target genes that are critical in thrombosis and inflammation, specific inhibitors of p50, such as Andro, may be therapeutically valuable for preventing and treating thrombotic arterial diseases, including neointimal hyperplasia in arterial restenosis.