Primary pulmonary leiomyosarcoma: A case report.

Primary pulmonary leiomyosarcoma (PPL) is an extremely rare malignant tumor. It has been revealed that PPL may originate from the smooth muscle of the pulmonary parenchyma, pulmonary arteries and bronchi. Patients with PPL may be asymptomatic or present with symptoms similar to those observed in other primary lung tumors. The present study reports the case of a 48-year-old man who presented with a lung mass and underwent a right upper-middle lobe bronchoscope tumor resection. The patient was subsequently diagnosed with PPL. Following the bronchoscopic tumor resection, chemotherapy was administered to the patient; however, the patient succumbed to the disease after the second cycle of chemotherapy.

Anti-Inflammatory Effects of Monoammonium Glycyrrhizinate on Lipopolysaccharide-Induced Acute Lung Injury in Mice through Regulating Nuclear Factor-Kappa B Signaling Pathway.

The present study aimed to investigate the therapeutic effect of monoammonium glycyrrhizinate (MAG) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and possible mechanism. Acute lung injury was induced in BALB/c mice by intratracheal instillation of LPS, and MAG was injected intraperitoneally 1 h prior to LPS administration. After ALI, the histopathology of lungs, lung wet/dry weight ratio, protein concentration, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) in the BALF were measured by ELISA. The activation of NF-κB p65 and IκB-α of lung homogenate was detected by Western blot. Pretreatment with MAG attenuated lung histopathological damage induced by LPS and decreased lung wet/dry weight ratio and the concentrations of protein in BALF. At the same time, MAG reduced the number of inflammatory cells in lung and inhibited the production of TNF-α and IL-1ß in BALF. Furthermore, we demonstrated that MAG suppressed activation of NF-κB signaling pathway induced by LPS in lung. The results suggested that the therapeutic mechanism of MAG on ALI may be attributed to the inhibition of NF-κB signaling pathway. Monoammonium glycyrrhizinate may be a potential therapeutic reagent for ALI.

Salidroside attenuates chronic hypoxia-induced pulmonary hypertension via adenosine A2a receptor related mitochondria-dependent apoptosis pathway.

Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial remodeling mainly due to excess cellular proliferation and apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs). Salidroside, an active ingredient isolated from Rhodiola rosea is proposed to exert protective effects against PAH. However, the function of salidroside in PAH has not been investigated systematically and the underlying mechanisms are not clear. To investigate the effects of salidroside on PAH, the mice in chronic hypoxia model of PAH were given by an increasing concentration of salidroside (0, 16 mg/kg, 32 mg/kg, and 64 mg/kg). After salidroside treatment, the chronic hypoxia-induced right ventricular hypertrophy and pulmonary arterial remodeling were attenuated, suggesting a protective role played by salidroside in PAH. To explore the potential mechanisms, the apoptosis of PASMCs after salidroside treatment under hypoxia conditions were determined in vivo and in vitro, and also the mitochondria-dependent apoptosis factors, Bax, Bcl-2, cytochrome C, and caspase 9 were examined. The results revealed that salidroside reversed hypoxia-induced cell apoptosis resistance at least partially via a mitochondria-dependent pathway. In addition, salidroside upregulated the expression of adenosine A2a receptor (A2aR) in lung tissues of mice and in PASMCs in vitro after hypoxia exposure. Combined the evidence above, we conclude that salidroside can attenuate chronic hypoxia-induced PAH by promoting PASMCs apoptosis via an A2aR related mitochondria dependent pathway.

[The study of catheterization to measure ventricular pressure in mice through venous cannula in external jugular vein].

OBJECTIVE: To study a feasible method of measuring right ventricular pressure by catheterization in mice. METHODS: Measuring the right ventricular pressure and the pulmonary artery pressure by homemade PE pipe through venous cannula in external jugular vein, using catheterization in mice with powerlab multimodal biometric signal recording system. RESULTS: Forty-six out of 51 mice were experimented with this method smoothly and got a total success rate of 90.2%. Thirty of 33 normal mice and 16 of 18 mice with pulmonary arterial hypertension (PAH) were catheterized successfully. The right ventricular pressure were as follow: systolic blood pressure: (23.4 +/- 5.7) mmHg in normal group vs (32.2 +/- 2.8) mmHg in mice with PAH, diastolic blood pressure: (3.7 +/- 2.6) mmHg vs (3.8 +/- 2.0) mmHg, mean pressure: (12.0 +/- 3.7) mmHg vs (14.9 +/- 2.3) mmHg. After autopsy for those 5 failed cases, we found that 2 cases were into the inferior vena cava, another 2 cases pierced the right auricle and the last one punctured the axillary vein into the chest wall. CONCLUSION: Measuring the right ventricular pressure through venous cannula in external jugular vein with homemade PE pipe in mice gets not only a high success rate but also help to save time. Moreover, this method can be popularized easily. It is a good and feasible method for measuring right ventricular pressure in mice.