Objective To investigate a simple and safe method for correction of the flat nose tip with the short columella. Methods The flat nose tip with the extend strut graft was corrected by using the rib cartilage or Medpor and the secondary defect of columella was repaired with the free composite graft of ear lobe in 8 cases of rhinoplasties. Results The free composite graft of ear lobe survived well and the color was similar to the neighboring tissue. There was no obviously secondary deformation at the donor site in all the cases by following-up from 1 to 2 years. Conclusions It is a simple and effective method without secondary deformation to repair the short columella by using the free composite graft of ear lobe in rhinoplasty.

The action mechanism of matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinases-2 (TIMP-2) in the genesis, development and degeneration of haemangioma was investigated by detecting their expression in the tissue of haemangioma in different phases by using the immunohistochemistry. Fifty paraffin-embedded specimens of skin capillary haemangioma were collected, which were documented in the Department of Pathology, Renmin Hospital of Wuhan University from 2000 to 2006. All samples were stained by regular HE method, and proliferative cell nuclear antigen (PCNA) was tested by immunohistochemical S-P method. The samples were classified according to the Mulliken criteria and the expression pattern of PCNA. Immunohistochemical S-P method was applied to detect the expression of MMP-2 and TIMP-2 in proliferative and degenerative phases of cutaneous capillary haemangioma, and in normal skin tissues. In combination with the detection of the expression of factor VIII-related antigen, it was verified that in haemangioma tissues, the cells expressing MMP-2 and TIMP-2 were vascular endothelial cells. The MMP-2 and TIMP-2 expression was quantitatively analyzed by image analysis system (HPIAS-1000), and one-way ANOVA(107) and SNK(q) test were done to analyze average absorbance (A) and positive area rate of immunohistochemically positive particles by using SPSS11.5. The results showed: (1) Among 50 samples of haemangioma, there were 26 proliferative haemangiomas, and 24 degenerative haemangiomas, respectively; (2) The expression of MMP-2 was weak in normal vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression of MMP-2 in proliferative group was significantly higher than in degenerative group and control group (normal skin) (P<0.05), but there was no statistically significant difference between the latter two groups; (3) TIMP-2 was highly expressed in normal tissues, degenerative vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression level of TIMP-2 in proliferative phase was significantly lower than in degenerative phase (P<0.05), and the expression of TIMP-2 in proliferative phase was significantly different from that in degenerative phase and normal tissues (P<0.05). It was concluded that in proliferative phase of haemangioma, MMP-2 may promote over-proliferation of endothelial cells of haemangioma, and in degenerative phase, TIMP-2 can inhibit the proliferation of endothelial cells of haemangioma. The two substances play important roles in the genesis, development and degeneration of haemangiomas.

Objective To explore the methodology and the indications of applying the porous high-density polyethylene(Medpor)combined with auricular cartilage in nasal plasty.Methods A total of 36 cases of nasal plasty were treated with the 8.5 mm thick Medpor implant(speader strut graft)and combined with the auricular cartilage graft to highlight the nasal tip.Results All 36 cases were satisfactory with the effects,and there were no complications such as infection,exposure of the implants and so on.Conclusions Medpor can supply the powerful supporting strength to the nasal tip,and it is a safe,effective implant to rebuild the supporting constructions of nasal tip,especially suitable to correct the over-rotation of nasal tip,flat nasal tip,and short nose.

Objective To investigate the expression of survivin and its relationship with that of caspase-3 in two stages of hemangioma and normal skin, and to explore the role of survivin in the patho-genesis of hemangioma. Methods A total of 50 cases of human dermal hemangioma and 8 eases of normal skin were analyzed for expression of survivin and caspase-3 by immunohistochemistry. Results The posi-tive ratio and average light density of survivin were obviously higher in proliferative hemangioma (0.2449±0.0135,0.7246±0.0747) than that in involutional hemangioma (0.1648±0.0217,0.5592±0.1601) and normal skin (0.1789±0.0126,0.4626±0.0961) (P<0.01). On the contrary, the expression of easpase-3 was up-regulated in involutional hemangioma (0.2386±0.0175, 0.4378±0.0593). Analysis of data also showed that there was a negative correlation between the average light density of survivin and caspase-3 (r=-0.95,P<0.01). Conclusions Survivin plays an important role in the pathogenesis of hemangioma and has a negative relationship with easpase-3.

Objective To investigate the relationship between the expression of p63, p73 proteins and the development of hemangioma. Methods The immunohistochemical technique and quantitative image analysis were used to detect the expression of p63 and p73 proteins in 40 cases of capillary hemangioma and 20 specimens of normal skin. Results The absorbance value (mean ? SD) of p63 and p73 expression in normal skin tissue, proliferative phase of hemangioma and involuting phase of hemangioma were 0.923 ? 0.191 and 0.953 ? 0.120, 8.271 ? 1.953 and 6.408 ? 2.151, 0.920 ? 0.187 and 1.073 ? 0.516, respectively. The expression of p63 and p73 in proliferative phase of hemangioma was significantly increased as compared with those in involuting phase of hemangioma and normal skin tissue (P 0.05). Conclusions It is suggested that p63 gene is not a tumor suppressor gene but an oncogene in hemangioma and may contribute to the proliferation of endothelial cell and be associated with angiogenesis, and p73 may play an important role in the proliferation of hemangioma.

nioma endothelial cells.

Objective To investigate the function of Bcl-2 and Bax in the pathogenesis,development and regression of human hemangiomas.Methods We examined the expression of Bcl-2 and Bax in proliferating versus involuting human hemangioma tissues and normal skin tissues using immunohistochemical technique.Results The expression of Bcl-2 in proliferating hemangiomas was significantly higher than that in involuting hemangiomas and normal skin tissues(P＜0.01).No significant difference was found between the expression of Bcl-2 in involuting hemangiomas and that in normal skin tissues(P＞0.05).The expression of Bax in involuting hemangiomas was significantly higher than that in proliferating hemangiomas and normal skin tissues(P＜0.01);the expression of Bax in proliferating hemangiomas was significantly higher than that in normal skin tissues(P＜0.05).Conclusion Bcl-2 and Bax participate in the development and involution of hemangioma,Bcl-2 plays a role in accelerating the proliferation of hemangioma by inhibiting the apoptosis of endothelial cells,and Bax promotes the switching from proliferation to involution in hemangiomas through inducing the apoptosis of endothelial cells.

In order to investigate the angiogenic effect of intercellular adhesion molecule-1 (ICAM-1), two parts of experiment were performed. Chick embryo chorioallantoic membrane (CAM) assay was used for in vivo angiogenic research. The chick embryos were divided into 4 groups: ICAM-1 group (divided into 3 subgroups, I, II and III) for screening the angiogenic effect of ICAM-1 by adding different concentrations of ICAM-1 (0.1, 0.2 and 0.3 microg/microL) 5 microL into the chick embryo CAMs on the day 10 after incubation for every subgroup; Anti-ICAM-1 group A (divided into 2 subgroups, I and II) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 microL into the chick embryo CAMs on the day 10 after incubation for every subgroup to evaluate the effect of ICAM-1 on the survival of microvessels through observing whether Anti-ICAM-1 could induce involution of the microvessels on CAMs; Anti-ICAM-1 group B (divided into 2 subgroups, I and II) by adding different concentrations of Anti-ICAM-1 (1:100, 1:50) 5 microL into the chick embryo CAMs on the day 6 after incubation for every subgroup to evaluate whether ICAM-1 involved in embryonic angiogenesis through observing the growth of microvessels on CAMs; Control group: ICAM-1 or Anti-ICAM-1 was substituted by PBS 5 muL on the day 10 or day 6 after incubation. Three days later, the CAMs were photographed in vivo, excised, sectioned and the number of microvessels was counted. In ICAM-1 group, there was increased number of microvessels arranged radially with "spoked-wheel" pattern around the gelatin sponges. The new microvessels growing perpendicularly to gelatin sponges were observed. The number of the microvessels growing in the CAM mesenchymes around the sponges in 3 subgroups was higher than that in control group (P<0.01), however, there was no significant difference among the 3 subgroups (P>0.05). In anti-ICAM-1 group A, the radially arranged microvessels were very unclear around the sponges contrast to that of ICAM-1 group. Few new microvessels were detected in the center of the sponges. The number of the microvessels growing in the CAM mesenchymes around the sponges in subgroup II was lower than that in control group (P<0.01). There was no significant difference in the number of the microvessels around the sponges between subgroup I and control group (P>0.05). In anti-ICAM-1 group B, the radially arranged microvessels were very unclear around the sponges contrast to that of control group. New microvessels were very scarce in the center of the sponges. The number of the microvessels growing in the CAM mesenchymes around the sponges in the 2 subgroups were less than that in control group (P<0.01), and there was significant difference between the 2 subgroups (P<0.05). It was suggested that ICAM-1 could induce angiogenesis and support the survival of microvessels, and ICAM-1 was involved in embryonic angiogenesis.

To explore the causes of the postoperative complications of the penile elongation and the measures to prevent them in order to raise the success rate of the penile elongation. 1,000 patients who had received the penile elongation were reviewed and analyzed for the causes of postoperative complications, and the measures of prevention and treatment were discussed. Our results showed that, of the 1,000 cases, 64 had the postoperative complications, including 20 cases of edema of prepuce, 15 cases of flap necrosis, 12 hematoma, 9 infections, and 8 cases of fat and clumsy penis. It is concluded that correct operative manipulation, strict aseptic measures and necessary postoperative care and management could avoid or reduce the postoperative complications. When complications happened, a satisfactory result can be achieved with timely and correct treatment in the majority of the patients.
Edema/etiology ; Edema/prevention & control ; Hematoma/prevention & control ; Penis/*abnormalities ; Penis/injuries ; Penis/*surgery ; Postoperative Complications/*prevention & control ; Postoperative Complications/therapy ; Reconstructive Surgical Procedures/methods ; Surgical Flaps ; Surgical Wound Infection/etiology ; Surgical Wound Infection/prevention & control ; Urologic Surgical Procedures, Male/methods

The action mechanism of matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinases-2 (TIMP-2) in the genesis, development and degeneration of haemangioma was in-vestigated by detecting their expression in the tissue of haemangioma in different phases by using the immunohistochemistry. Fifty paraffin-embedded specimens of skin capillary haemangioma were col-lected, which were documented in the Department of Pathology, Renmin Hospital of Wuhan University from 2000 to 2006. All samples were stained by regular HE method, and proliferative cell nuclear anti-gen (PCNA) was tested by immunohistochemical S-P method, The samples were classified according to the Mulliken criteria and the expression pattern of PCNA. Immunohistochemical S-P method was ap-plied to detect the expression of MMP-2 and TIMP-2 in proliferative and degenerative phases of cuta-neous capillary haemangioma, and in normal skin tissues. In combination with the detection of the ex-pression of factor Ⅷ-related antigen, it was verified that in haemangioma tissues, the cells expressing MMP-2 and TIMP-2 were vascular endothelial cells. The MMP-2 and TIMP-2 expression was quantita-tively analyzed by image analysis system (HPIAS-1000), and one-way ANOVA(107) and SNK(q) test were done to analyze average absorbance (A) and positive area rate of immunohistochemically positive particles by using SPSS11.5. The results showed: (1) Among 50 samples of haemangioma, there were 26 proliferative haemangiomas, and 24 degenerative haemangiomas, respectively; (2) The expression of MMP-2 was weak in normal vascular endothelial cells, cytoplasm of connective tissues and extracellu-lar matrix around blood vessels. The expression of MMP-2 in proliferative group was significantly higher than in degenerative group and control group (normal skin) (P<0.05), but there was no statisti-cally significant difference between the latter two groups; (3) TIMP-2 was highly expressed in normal tissues, degenerative vascular endothelial cells, cytoplasm of connective tissues and extracellular matrix around blood vessels. The expression level of TIMP-2 in proliferative phase was significantly lower than in degenerative phase (P<0.05), and the expression of TIMP-2 in proliferative phase was signifi-cantly different from that in degenerative phase and normal tissues (P<0.05). It was concluded that in proliferative phase of haemangioma, MMP-2 may promote over-proliferation of endothelial cells of haemangioma, and in degenerative phase, TIMP-2 can inhibit the proliferation of endothelial cells of haemangioma. The two substances play important roles in the genesis, development and degeneration of haemangiomas.