A Case of Pulmonary Embolism with Sarcomatoid Malignant Pleural Mesothelioma with Long-Term Pleural Effusion.

BACKGROUND: Malignant pleural mesothelioma (MPM) is a highly aggressive tumor that originates from pleural mesothelial cells. In recent years, with the development of asbestos-related industries and the increase in air pollution, its incidence has been increased. The incidence of pulmonary embolism combined with sarcomatoid MPM is very low and the prognosis is extremely poor. We here report a case of a patient with long term of pleural effusion and finally diagnosed as pulmonary embolism with sarcomatoid MPM. CASE: A 75-year-old male with a 30-year history of asbestos exposure was admitted to our hospital due to chest pain and difficulty in breathing after exercise. Radiologic examination revealed pleural effusion, computed tomography pulmonary angiography (CTPA) suggests pulmonary embolism, and we consider pleural effusion caused by pulmonary embolism. After anticoagulant therapy for pulmonary embolism and pleural puncture to reduce pleural effusion, the patient's symptoms improved. However, after that, the patient was still admitted to the hospital several times because of recurrent chest pain and dyspnea symptoms, and radiologic examination always showed unexplained pleural effusion. Finally, pathological and immunohistochemical examinations of the pleural biopsy specimens were performed, and the diagnosis was confirmed as sarcomatoid MPM. CONCLUSION: In summary, sarcomatoid MPM with pulmonary embolism is relatively rare, and the prognosis is poor. Clinicians need to be alert to its occurrence. When the first diagnosis is confirmed and the effect of targeted treatment is still not good, the possibility of other diseases should be considered. In clinical practice, pleural biopsy guided by PET-CT is a good choice for patients with sarcomatoid MPM who cannot tolerate open pleural biopsies or thoracoscopy. And patients should undergo pleural morphology and immunohistochemistry as soon as possible, which are helpful for timely diagnosis.

Effects of genistein on lipopolysaccharide-induced injury of mouse alveolar epithelial cells and its mechanism.

Alveolar and bronchial epithelial cells have critical functions in acute respiratory distress syndrome progress. Genistein could protect the lungs from acute lung injury, however, whether genistein protects the alveolar epithelial cells from LPS-induced injury was less studied. Spectrophotometric method 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and enzyme-linked immunosorbent assay (ELISA) were performed to detect cell viability and levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6. Flow cytometry and western blot assay were performed to detect cells apoptosis and protein levels. In LPS-induced model of mouse lung epithelial (MLE)-12 cells, PBEF (proinflammatory cytokine) expression, and cell apoptosis were increased and cell viability was decreased, whereas NF-κB was activated and expression levels of TNF-α, IL-1ß, and IL-6 were increased. However, genistein partly reversed the effect of LPS, and it plays a protective role in lung injury by reducing expression of PBEF, inhibiting the activation of NF-κB and alleviating inflammatory response of cells.

A Rare Case Of Synchronous Multiple Primary Lung Cancer: Squamous Cell Cancer And Small Cell Lung Cancer.

The incidence of synchronous multiple primary malignancies has been reported to be low. We report a rare case of synchronous lung squamous cell cancer and small cell lung cancer in an 82-year-old male patient. There is a lack of standard diagnostic criteria for multiple primary lung cancer. Two tumors with similar morphology are difficult to draw conclusions about the same lineage or different lineages. If the patient's physical condition permits, multiple tumors should be sampled and tested. Besides, imaging features are helpful for identification. It is advisable to diagnose synchronous multiple primary malignancies in an early stage, which contributes to a favorable outcome.

Lentivirus-mediated disintegrin and metalloproteinase 17 RNA interference reversed the acquired resistance to gefitinib in lung adenocarcinoma cells in vitro.

OBJECTIVE: The aim of the study is to evaluate the effects of silencing a disintegrin and metalloproteinase 17 (ADAM17) gene expression by lentivirus-mediated RNA interference (RNAi) in the gefitinib-resistant lung adenocarcinoma cells, and then to explore whether the recombinant lentivirus mediated ADAM17 RNAi reversed the acquired resistance of lung adenocarcinoma to gefitinib in vitro. METHODS: The gefitinib-resistant RPC-9 cells were established and the mutations of EGFR were detected by gene sequencing. The ADAM17 shRNA expression vectors were constructed and packaged to recombinant lentivirus. The cell proliferation viability was detected by MTT, and cellular apotosis was analyzed by flow cytometry assay. The expression levels of ADAM17, EGFR and the phosphorylated EGFR were respectively detected by reverse transcription polymerase chain reaction and western blot. TGF-α production in the supernatant was detected by enzyme-linked immunosorbent assay. RESULTS: The gefitinib-resistant RPC-9 cells in which mutated EGFR (exon 20) carried 790T > T/M mutation were established. When the concentrations of gefitinib were less than 10µmol/L, there were no significant changes in the apoptosis and cellular proliferation of RPC-9 with the dose-escalation of gefitinib. The cell proliferation viability of RPC-9 was significantly decreased by lentivirus mediated ADAM17 RNAi (P < 0.05). Gefitinib did not inhibit ADAM17 expression in both the gefitinib-sensitive PC-9 and gefitinib-resistant RPC-9 cells (P > 0.05). Gefitinib had no significant effects on TGF alpha production in the supernatants (P > 0.05). Gefitinib did not inhibit EGFR expression in gefitinib-sensitive PC-9 and gefitinib-resistant RPC-9 cells (P > 0.05). The phosphorylation of EGFR in gefitinib-sensitive PC-9 cells was significantly inhibited by gefitinib (P < 0.05), but that in gefitinib-resistant RPC-9 could not be inhibited by gefitinib (P > 0.05). Lentivirus mediated ADAM17 RNAi significantly inhibited the mRNA and protein expression of ADAM17 in gefitinib-resistant RPC-9 cells (P < 0.05), as well as TGF alpha production in the supernatants (P < 0.05). Also, the phosphorylation of EGFR was significantly reduced in gefitinib-resistant RPC-9 cells by lentivirus mediated ADAM17 RNAi (P < 0.05); however, the mRNA and protein expression of EGFR could not be inhibited. CONCLUSION: Lentivirus mediated ADAM17 RNAi may reverse the acquired resistance of lung adenocarcinoma to gefitinib via inhibiting the upstream of EGFR signal pathway, which may provide a new therapeutic target to solve the acquired resistance to EGFR tyrosine kinase inhibitors in lung adenocarcinoma. © 2017 American Institute of Chemical Engineers Biotechnol. Prog., 34:196-205, 2018.

Solely lung-involved IgG4-related disease : a case report and review of the literature.

By analyzing the clinical data of 1 case of IgG4-related lung disease(IgG4-RLD) and the review of literature, the author investigated the clinical characteristics of IgG4-RLD. IgG4-RLD is a rare disease characterized by significant elevation of serum IgG4 and infiltration of a large number of IgG4+ plasma cells. The clinical manifestations of the disease were nonspecific, and the imaging features were mixed with several types. The disease can only be involved in the lung, but also multiple organ involvement. Solely lung-involved IgG4-RD is not only extremely rare but also easily misdiagnosed as tuberculosis, lung cancer, lymphoma and other common pulmonary diseases. Histopathological examination is the key to the diagnosis of the disease. Corticosteroids are the first choice of treatment, and the overall prognosis is good.

[Application of Neuroform stent in the treatment of intracranial aneurysm].

OBJECTIVE: To introduce the application of Neuroform stent in the treatment of intracranianl wide neck aneurysm. METHODS: Eight patients (9 aneurysms), including 3 males and 5 females, aged from 41 to 74, were treated. Among the 9 aneurysms, there were 3 wide-neck aneurysms in internal carotid artery (ICA), 4 vertebral aneurysms (in 3 cases), and 2 basilar tip giant aneurysms. Heparinization were given for all procedures after femoral artery Seldinger's puncture. Stents were released through 3 m Transcend 0.014 guide wires, which were posited in the aneurysm-carry arteries first, or, through a 205 cm Transcend 0.014 guiding wire. Further coiling was selected for some cases. After the treatment 24 h heparinization were maintained. For coiling cases, aspirin (300 (mg/d) and ticlopiding (250 mg/d) were given at first 6 weeks, and aspirin (300 mg/d) was given following 6 months. For stent alone cases, only 1 month aspirin (300 mg/d) was given. RESULTS: In one ICA aneurysm, the stent moved to the bifurcation of ICA while a coil was pushed into the aneurysm lumen, and the ICA spasmed. Partial occlusion achieved in the aneurysm. The patient died due to bleeding of the aneurysm 20 h after anticoagulation treatment with heparin. One dissection aneurysm and 2 fusiform aneurysms (in bilateral vertebral arterys of one patient) were treated with stents only. The dissection aneurysm was completely occluded after 3 months. In 1 basilar artery (BA) tip giant aneurysm, the distal part of BA spasmed immediately after stenting. Complete occlusion was achieved with coils 4 months later. Another BA tip aneurysm was partially occluded after the stent was deployed. The other 3 aneurysms were completely embolized with the protection of the Neuroform stents. There is no further DSA follow-up of the cases. CONCLUSIONS: The Neuroform stent is easy to pass through the tortuous vessels. Combine with coils, it may be used in the treatment of wide neck aneurysms. However, it has the risk of migration because of the softness.