Objective To analyze the clinical feature of thalassemia with pulmonary hypertension and investigate the influence of pulmonary hypertension on thalassemia.Methods From June 2007 to July 2011,clinical data of 19 patients with thalassemia complicated with pulmonary hypertension in TEDA International Cardiovascular Hospital of Tianjin Medical University and Affilated Hospital of Guilin Medical College were analyzed retrospectively.Twenty-two cases of thalassemia without pulmonary hypertension were as a control group,and follow-up time was set as 4 months to 24 months.Observed indicators included age,hemoglobin(Hb),lactate dehydrogenase (LDH),serum ferritin (SF),tricuspid regurgitation velocity (TRV) and left ventricular ejection fraction (LVEF).Results SF and TRV of the case group[(693.6 ± 234.6)μg/L and (2.6 ± 0.1)m/s] were significantly higher than those of the control [(209.5 ± 100.1) μg/L and (2.1 ± 0.3)m/s,all P ＜ 0.05]; but the differences between case and control group in Hb[(90.8 ± 10.7)g/L vs (89.3 ± 10.5)g/L],LDH[(320.9 ± 103.7)U/L vs (355.8 ± 140.3)U/L] and LVEF[(66.2 ± 7.1)％ vs (64.2 ± 4.7)％] were not statistically significant (all P ＞ 0.05).Logrank analysis showed that the prognosis was poor in patients with thalassemia complicated with pulmonary hypertension (x2 =4.95,P ＜ 0.05).Multiple regression analysis indicated that age and serum ferritin remained as predisposing risk factors for tricuspid regurgitation velocity,and serum ferritin had a greater impact on the velocity.Conclusion In patients with thalassemia complicated with pulmonary hypertension,the prognosis is poor; age and SF may be factors involved in the development of pulmonary hypertension.

BACKGROUND:Effects of different oxygen partial pressures on cytokine secretion of human adipose-derived stem cells have been differently reported. These differences may be caused by varying oxygen partial pressures.
OBJECTIVE:To investigate the influence of different oxygen partial pressures on cytokines secreted from human adipose-derived stem cells.
METHODS:Human adipose-derived stem cells were cultured in vitro and identified by its immunophenotype. Human adipose-derived stem cells were divided into five groups and cultured under different oxygen partial pressure conditions (1%, 3%, 5%, 10%, 21%) for 24 hours, respectively. With quantitative real-time PCR and enzyme linked immunosorbent assay, the secretion of cytokines, vascular endothelial growth factor, hepatocyte growth factor, nerve growth factor, keratinocyte growth factor, from human adipose-derived stem cells were analyzed on the gene and protein levels.
RESULTS AND CONCLUSION:Human adipose-derived stem cells were positive for CD71, CD73, CD90, CD105 and negative for CD34, CD45, CD54, HLA-DR. From the aspect of gene level, hypoxia (1%, 3%O 2 ) promoted the expression of vascular endothelial growth factor and nerve growth factor from human adipose-derived stem cells (P<0.01), and significantly elevated the expression of hepatocyte growth factor (P<0.05);however, there was no significant influence on keratinocyte growth factor under hypoxia (P>0.05). Based on the protein level, protein secretion of hepatocyte growth factor and vascular endothelial growth factor from human adipose-derived stem cells was increased under hypoxia (P<0.01), but no changes occurred in nerve growth factor and keratinocyte growth factor. After cultured under hypoxic environment, human adipose-derived stem cells were promoted to express gene vascular endothelial growth factor, hepatocyte growth factor and nerve growth factor, as wel as to secrete protein keratinocyte growth factor and vascular endothelial growth factor.

BACKGROUND: Our former studies have shown that bone marrow mesenchymal stem cells (BMMSCs) can be induced differentiation to vascular smooth muscle-like cells (VSMLCs) and vascular endothelium-like cells (VELCs), which are compatible with collagen-embedded polyglycolic acid scaffolds. OBJECTIVE: To investigate the possibility of constructing small diameter tissue-engineered blood vessels via subcutaneous implantation. METHODS: The cells-scaffold complex was produced by separately seeding VSMLCs and VELCs derived from BMMSCs on polyglycolic acid collagen scaffolds. The two layers were separated by ECMgel. The cells-scaffold complex was subcutaneous implanted into small diameter tissue-engineered blood vessels.RESULTS AND CONCLUSION: Histological analysis of the small diameter tissue-engineered blood vessel walls revealed a typical artery structure, which was similar to natural vessels. The tissue-engineered blood vessels were not broken down under a force of 26.6 kPa. Eight weeks after implantation, the Brdu-labeled seed cells were found in the three layers of the vessel walls. The results revealed that the subcutaneous tissue was a good bioreactor to construct small diameter tissue-engineered blood vessels.

Objective To investigate the detailed molecular mechanism of matrix stiffness regulating cell drug resistance. Methods Polyacrylamide hydrogels of soft substrate (10 kPa), hard substrate (38 kPa) and rigid substrate (57 kPa) with different matrix stiffness were configured to simulate the physical matrix stiffness at different stages of breast cancer in vivo. Results The cell proliferation rate of the hard substrate was significantly higher than that of the soft and rigid substrates. The intracellular endocytosis was significantly lower on the hard substrate. The YAP nucleus translocation increased significantly on the hard substrate, compared with the soft and the rigid substrates, indicating that YAP was a key molecule involved in drug resistance of tumor cells. Conclusions Matrix stiffness could regulate the drug resistance of breast cancer cells through YAP activation. This study not only provides a new direction for elucidating the mechanism of drug resistance, but also lays a new foundation for the drug delivery system of breast cancer treatment.