OBJECTIVETo investigate the significance of beta-adrenergic receptor 2 (beta2-AR) and vascular endothelial growth factor-2 (VEGFR-2) in the occurrence and development of infantile hemangioma through detecting the expression of beta2-AR and VEGFR-2 in the different stages of infantile hemangiomas.

METHODSAccording to the Mulliken's classification standard, we classified the specimens as proliferating group (32 cases), involuting group (17 cases) and involuted group (11 cases). Normal skin tissue surrounding the hemangioma from 7 cases were chosen as control group. The expression of beta2-AR and VEGFR-2 was detected by immunohistochemical technique in proliferating hemangioma, involuting hemangioma, involuted hemangioma. The mean optical density was measured by image analysis system (Image Pro Plus 6.0) and SPSS 16.0 software was applied for statistical analysis.

RESULTSThe expression of beta2-AR and VEGFR-2 was strongly positive in proliferating hemangioma, while positive in involuting hemangioma and weakly positive in the involuted stage. The mean optical density of each phase was 0.064 751 2 +/- 0.012 747, 0.031 6017 +/- 0.006 848,0.011 869 8 +/- 0.039 349 for beta2-AR, and 0.068 940 9 +/- 0.029 274, 0.028 445 5 +/- 0.006 396, 0.011 184 1 +/- 0.004 198 for VEGFR-2. The differences between different stages had a statistically significance (P < 0.05). Correlation analysis on the mean optical density between beta2-AR and VEGFR-2 had a statistically significance (P < 0. 05).

CONCLUSIONSBeta2-AR and VEGFR-2 may be involved in the occurrence and development of infantile hemangioma.

Child ; Child, Preschool ; Female ; Hemangioma ; metabolism ; Humans ; Infant ; Male ; Receptors, Adrenergic, beta-2 ; metabolism ; Receptors, Vascular Endothelial Growth Factor ; metabolism

BACKGROUND:The homing ability of mesenchymal stem cells is closely associated with the effects of celltransplantation. Clarifying the mechanism of chemotaxis and migration wil contribute to enhance the clinical application of mesenchymal stem cells. OBJECTIVE:To investigate the effect of Cdc42 in the homing of human umbilical cord mesenchymal stem cells. METHODS:First, mesenchymal stem cells were isolated from human umbilical cord, and co-cultured with tumor necrosis factorα, interleukin-1β, and transforming growth factorβ. Western blot assay was used to test the level of Cdc42. Besides, Cdc42 siRNA was synthesized by chemical method to transfect the cells, and cellmigration and adhesion were measured by Transwel and Matrigel separately. Meanwhile, the activity of signal molecule, extracellular regulated protein kinase 1/2, was evaluated by western blot. RESULTS AND CONCLUSION:The results indicated that the inflammation factors induced the highly expression of Cdc42 in human umbilical cord mesenchymal stem cells, almost double level to controls. siRNA notably inhibited the migration and adhesion of human umbilical cord mesenchymal stem cells through Cdc42 down-regulation, and the extracellular regulated protein kinase 1/2 and phosphorylation form were also decreased simultaneously. In a word, we speculate Cdc42 plays a role in the chemotaxis of human umbilical cord mesenchymal stem cells in vitro.

Objective To study the protective effect of glucocorticoid preconditioning on the myocardial ischemic and reperfused hearts.Methods Totally 18 rabbits were randomly divided into three groups: myocardial ischemia-reperfusion model(model),high-dose glucocorticoid given by one time group(high-dose group) and low-dose glucocorticoid given by several times group(low-dose group),with six rabbits in each group.Myocardial ischemia was induced by left anterior descending coronary artery ligation.ST segments were recorded by the BL-420 biological signal acquisition system.Plasma malondial dehyde(MDA) was examined before ischemia,at 15 min after ischemia and 30 min after reperfusion;ischemic heart muscles were prepared with cryotomy and stained histochemically.Succinic dehydrogenase activity was observed in the ischemic region.Results There was shorter time of ST-segment recovery in the high-dose group and the low-dose group than that in the model group.Serum level of MDA in the high-dose group was lower than in the low-dose group(P

Early-onset scoliosis (EOS) is defined as the scoliosis occurs before 10 years old. Such patients with severe scoliosis often require early surgical intervention, but spinal fusion may also affect their thoracic development and lung function. Based on etiology, EOS can be classified as congenital, neuromuscular, syndrome-related and idiopathic scoliosis. The clinical goal is to control the progression of the curve while allowing the spine and chest to grow as much as possible to promote the development of alveolar. Clinical treatments include physiotherapy, plaster and brace correction as well as surgery. Patients of EOS were usually at the critical stage of thoracic and lung development due to their young age. In addition, the combination of severe thoracic deformity may also lead to life-threatening cardiopulmonary disorder and related complications considering the clinical inconsistency and complexity of EOS. Thoracic anatomical changes brought by scoliosis itself can limit chest wall movement and reduce lung compliance, resulting in changes in thorax diameter and compression of thoracic volume, leading to restrictive ventilation dysfunction. And spinal fusion can effectively correct curve and control progression, which still remains as the primary surgical option for severe EOS patients nowadays. However, early spinal fusion can also lead to deformation of lung tissue, collapse and malformation of alveolar while limiting the height and growth rate of thoracic cavity, hindering the circulatory system and leading to respiratory dysfunctionof children. Spinal growth restriction, crankshaft phenomenon and restricted alveolar proliferation may play a role in thisprocess. The present review retrospectively summarized the effects and possible mechanisms of early spinal fusion on lung function and thoracic development in patients with EOS, aiming to further provide guidance for clinical decisions.

Objective To evaluate the specific antibody-producing capacity of locally infiltrating B lymphocytes in lesions of patients with pemphigus vulgaris (PV).Methods Totally,35 patients with PV and 22 healthy controls were enrolled into this study.Skin tissues were resected from blisters or erosions of the patients with PV,and from normal skin of healthy controls.Then,mononuclear cells were isolated from these skin tissues.Flow cytometry was performed to determine the percentages of lymphocytes,CD 19+ B lymphocytes,and desmoglein (Dsg)1-and Dsg3-specific CD19+ B lymphocytes.B lymphocytes isolated from the lesional skin of patients with PV were cultured in vitro.Enzyme-linked immunosorbent assay (ELISA) was conducted to determine titers of anti-Dsg1 and anti-Dsg3 antibodies in the cell culture supernatant.Receiver operating characteristic (ROC) curve analysis was conducted to calculate positive rates of anti-Dsg1 and anti-Dsg3 antibodies.Results The percentages of lymphocytes (17.95％ ± 3.85％) and CD19+ B lymphocytes (4.27％ ± 1.13％) were significantly higher in the lesional skin of PV patients than in the normal skin of healthy controls (7.83％ ± 1.29％,0.61％ ± 0.31％ respectively;t =2.49,U =13.00 respectively,both P ＜ 0.05).Among the CD19+ B lymphocytes in the lesional skin of PV patients,the percentage of CD19qgG+ B cells was (38.33 ± 5.56)％,and percentages of Dsg1-and Dsg3-specific CD19+ B lymphocytes were 12.87％ ± 1.267％ and 10.42％ ± 1.243％ respectively.After the in vitro culture for 6 days,the titers of anti-Dsg1 and anti-Dsg3 antibodies in the cell culture supematant were (4.89 ± 1.56) U/ml and (35.45 ± 13.03) U/ml respectively,with their positive rates being 85％ (17/20)and 95％ (19/20) respectively.Conclusion There are Dsg1-and Dsg3-specific B lymphocytes aggregating in the lesional skin of patients with PV,which can produce anti-Dsg1 and anti-Dsg3 antibodies after in vitro culture.

【Objective】 To analyze the causes of a case of hemolytic disease of the fetus and newborn (HDFN),and investigate the genetic background of maternal Rh deletion D--formation. 【Methods】 Blood samples of maternal and fetus were collected, and ABO blood typing, Rh blood typing, antibody screening and identification test were performed to explore the blood group serological characteristics of Rh deletion type D--, and Rh gene sequence was performed on parturient. 【Results】 The maternal blood group was identified to be O type, D--, and the anti-Hr0 antibody against Rh high-frequency antigen was suspected to be caused by multiple pregnancies which passes through the placental barrier and enable fetus to obtain anti Hr0 antibody, leading to HDFN, with genetic testing result as RH RHCE* Ce/RHCE* Ce. 【Conclusion】 In-depth research on the formation mechanism of Rh D-- in parturient should be conducted to provide clinical value for HDFN blood exchange treatment and blood transfusion in special blood group population.