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Background: Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare malignancy-related respiratory complication, demonstrating rapid progression of pulmonary hypertension (PH) and respiratory failure. Although a number of treatments have been attempted for patients diagnosed with or suspected of having PTTM, successful-treated cases of PTTM were mainly from imatinib therapy, which was a PDGF receptor inhibitor. Anlotinib was a novel tyrosine kinase inhibitor that targets VEGFR, FGFR, PDGFR, and c-kit., Case Presentation: We reported a patient of PTTM associated with gastric carcinoma, whom were treated with anlotinib, thereby exhibiting significant improvement of PH and respiratory dysfunction., Conclusion: Our case provides a new understanding of therapy to PTTM, with implications for defining anlotinib as candidate drug for PTTM. Clinical diagnosis and prompt initiation of anlotinib might be one of the strategies in patients with unstable PTTM., (© 2023. The Author(s).)

Background: Colorectal cancer (CRC) is one of the most malignant cancers worldwide. Nonylphenol (NP) is an endocrine-disruptor chemical and plays an important role in the development of cancers. However, the effects of NP on CRC remain unclear. In this study, we aimed to investigate the potential mechanisms of NP in the pathogenesis of CRC., Methods: The levels of AhR, TL1A and HDAC2 in CRC tissues and endothelial cells were assessed by RT-qPCR or western blot. CHIP and dual luciferase reporter assays were used to confirm the interaction between AhR and HDAC2, or HNF4α and TL1A. The CCK8, would healing and tube formation assays were conducted to evaluate the proliferation, migration and angiogenesis of HUVECs. Western blot determined HNF4α protein and HNF4α acetylation levels. The secreted TL1A protein was detected by ELISA. The angiogenesis-related factor CD31 was tested by IHC., Results: The expression level of AhR was significantly up-regulated in CRC tissues and endothelial cells. Moreover, NP activated the AhR pathway mediated colorectal endothelial cell angiogenesis and proliferation, while TL1A overexpression resisted these effects caused by NP. Besides, NP was found to modulate HNF4α deacetylation through AhR/HDAC2 to inhibit TL1A. Furthermore, in vivo experiments proved that NP regulated CRC growth and angiogenesis via AhR/HDAC2/HNF4α/TL1A axis., Conclusion: This study revealed that NP promoted CRC growth and angiogenesis through AhR/HDAC2/HNF4α/TL1A pathway and could be a new therapeutic target for CRC treatment., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objective: To improve the clinical management of acute pulmonary embolism caused by antithrombin Ⅲ (AT Ⅲ) deficiency through gene sequence analysis of the SERPINC1 gene. Methods: The diagnosis and treatment of a 33-year-old male patient with chest pain was reviewed. All exon sequences and flanking regions of 7 related genes of thrombophilia were subjected to detection by high-throughput next generation sequencing technology. The gene mutation was inquired in the gene database and the pathogenic probability of the mutant gene was predicted by Mutation Taster software. Results: The patient was diagnosed with acute pulmonary embolism (intermediate-low risk), with the ATⅢ activity less than 50%. Anticoagulation with nadroparin calcium combined with warfarin was administrated, but hemoptysis was aggravated, and then the medication was replaced by anticoagulant of rivaroxaban. In the end, the embolus was gradually absorbed. A heterozygous missense mutation of c.1148T>A (p.L383H) in the SERPINC1 gene was detected. The gene database and Mutation Taster confirmed the mutation as a new pathogenic mutation with the pathogenic probability of 0.999 999 851 200 991. Conclusions: C.1148T>A (p.L383H) is a novel pathogenic mutation in SERPINC1 gene that complements and updates the gene mutation spectrum of hereditary AT Ⅲ deficiency. The new oral anticoagulant rivaroxaban may be used as the first-line treatment for these patients.

Here, we report a case of adenoviral pneumonia associated with critical ARDS treated with Cidofovir, prone ventilation and extracorporeal membrane oxygenation (ECMO). The patient responded well to therapy and recovered without further complications. Cidofovir, with early prone ventilation and ECMO support, may be a therapeutic option for patients with critical ARDS related to adenoviral pneumonia., (© 2020 John Wiley & Sons Ltd.)

Objective: To evaluate the inhibitory effect of Nandeshi, an acrosin inhibitor, on human acrosin activity., Methods: We collected sperm samples from 10 healthy fertile men and cultured them with Nandeshi at 30 degrees C for 5 minutes at the concentrations of 0. 100, 0.120, 0.144, 0.173, 0.207, 0.249, 0.299, 0.358 and 0.430 mmol/L, with the controls treated with a well-known acrosin inhibitor N-alpha-p-tosyl-L-lysine chloromethylketone (TLCK) at 150.0, 189.8, 213.6, 240.3, 270.3, 304.1 and 342.1 mmol/L. Then we determined the residual activity of human acrosin by improved Kennedy assay., Results: The residual activity of acrosin was negatively correlated with the Nandeshi concentration, and Nandeshi exhibited an inhibition rate about 800 times that of TLCK., Conclusion: Nandeshi has a powerful inhibitory effect on human acrosin, and improved Kennedy assay is a simple, practical and highly sensitive technique for the detection of human acrosin activity.