Anti-tumor effect of Liqi, a traditional Chinese medicine prescription, in tumor bearing mice

<p>Abstract</p> <p>Background</p> <p><it>Liqi</it>, an herbal preparation used in traditional Chinese medicine, has been used to treat cancer in China for centuries. We investigated the anti-tumor effects of liqi and their mechanisms in mice that had been xenografted with tumors.</p> <p>Methods</p> <p>Sarcoma 180 tumor, Lewis lung carcinoma, and SGC-7901 cells were implanted in BALB/c mice, C57BL/6 mice, and BALB/c nude mice, respectively. Liqi was administered to subgroups of these mice. The tumor weight and size were measured. Cell cycle analysis and T lymphocyte subsets were determined by flow cytometry. The activity of NK cells and TNF was tested using cytotoxicity assay on YAC-1 cells and L929 cells, respectively, and the activity of IL-2 was tested with an IL-2-dependent CTLL-2 cell proliferation assay. Platelet aggregation was monitored by measuring electric impedance, and the levels of thromboxane A2 (TXA₂) and prostacyclin (PGI₂) in blood were measured by ¹²⁵I-TXB₂and ¹²⁵I-Keto-PGF_1αradioimmunoassay.</p> <p>Results</p> <p>The results showed that liqi inhibited tumor growth in tumor-implanted mice and arrested the cell proliferation in the G0/G1 phase and reduced the portion of cells in S and G2/M phase for SGC-7901 cells. Liqi increased the activity of NK cells and TNF-α, stimulated IL-2 production and activity, and regulated T lymphocyte subpopulations. Liqi inhibited the Lewis lung carcinoma metastasis by inhibiting platelet aggregation and normalizing the balance between TXA₂and PGI₂.</p> <p>Conclusion</p> <p>All these findings demonstrated that liqi has an anti-tumor effect in vivo. The mechanism may be related to immune regulation and anticoagulation effects.</p

A review of outcome following valve surgery for rheumatic heart disease in Australia

Background: Globally, rheumatic heart disease (RHD) remains an important cause of heart disease. In Australia it particularly affects younger Indigenous and older non-Indigenous Australians. Despite its impact there is limited understanding of the factors influencing outcome following surgery for RHD. Methods: The Australian and New Zealand Society of Cardiac and Thoracic Surgeons Cardiac Surgery Database was analysed to assess outcomes following surgical procedures for RHD and non-RHD valvular disease. The association with demographics, co-morbidities, pre-operative status, valve(s) affected and operative procedure was evaluated. Results: Outcome of 1384 RHD and 15843 non-RHD valve procedures was analysed. RHD patients had longer ventilation, experienced fewer strokes and had more readmissions to hospital and anticoagulant complications. Mortality following RHD surgery at 30 days was 3.1 % (95 % CI 2.2 – 4.3), 5 years 15.3 % (11.7 – 19.5) and 10 years 25.0 % (10.7 – 44.9). Mortality following non-RHD surgery at 30 days was 4.3 % (95 % CI 3.9 - 4.6), 5 years 17.6 % (16.4 - 18.9) and 10 years 39.4 % (33.0 - 46.1). Factors independently associated with poorer longer term survival following RHD surgery included older age (OR1.03/additional year, 95 % CI 1.01 – 1.05), concomitant diabetes (OR 1.7, 95 % CI 1.1 – 2.5) and chronic kidney disease (1.9, 1.2 – 2.9), longer invasive ventilation time (OR 1.7 if greater than median value, 1.1– 2.9) and prolonged stay in hospital (1.02/additional day, 1.01 – 1.03). Survival in Indigenous Australians was comparable to that seen in non-Indigenous Australians.Conclusion: In a large prospective cohort study we have demonstrated survival following RHD valve surgery in Australia is comparable to earlier studies. Patients with diabetes and chronic kidney disease, were at particular risk of poorer long-term survival. Unlike earlier studies we did not find pre-existing atrial fibrillation, being an Indigenous Australian or the nature of the underlying valve lesion were independent predictors of survival