We observed the changes of IOP after contact transscleral cyclophotocoagualtion with Diode laser which emit 810mm beam and we tride to investigatethe suitable level and range of energy when Diode laser was applied to the refractory glaucoma patients. Fifteen eyes underwent contact transscleral cyclophotocoagulation with energy 3J(Group A, 6eyes), 4J(Group B, 9eyes) separately and intraocular pressure(IOP) was measured at 1 day, 1 week, 1 month, 2 month, 3 month, 4month, 5month, 6month, postoperatively. The intraocular pressure(IOP) decreasing rate was 83.02% in A group and 64.72% in B group. The success rate was 50% in A group and 66.7% in B group at 6 month postoperatively. It is suggested that contact transscleral cyclophotocoagulation with Diode laser si useful in lowering IOP in refractory glaucoma patients.
Glaucoma* ; Humans ; Lasers, Semiconductor*

We investigated the outcome of needling revision with adjunctive subconjunctival 5-fluorouracil(5-FU) injection performed on 20 eyes of 20 consecutive glaucoma patients with failed filtering blebs. Follow-up time was 44.5+/-53.9 weeks from the first needling revision and 31.8+/-43.5 weeks from the last needling procedures. We divided the patients into the success group and the failed group depending on the change of the intraocular pressure(IOP) after needling, and analysed the multi-factors which influenced the success rate of needling by logistic regression analysis. Thirteen(65%) of the eyes were classified treatment success after 1.6+/-0.8 needling revision, with a mean intraocular presure(IOP) of 19.8+/-1.9mmHg on 1.1+/-0.9 medications, significantly lower mean IOP and number of medications than before the procedure(28.1+/-15.7mmHg [P<0.01, paired t-test]). Needling revision with adjunctive 5-FU appears to be a safe and effective means of reestablished filtration.
Blister* ; Filtration ; Fluorouracil ; Follow-Up Studies ; Glaucoma ; Humans ; Logistic Models ; Trabeculectomy*

It is been known that the deltoid ligament of the ankle joint plays an important role in the stabiliy of the ankle joint. In cases of deltoid ligament rupture, associated with lateral malleolar fractures, cannot be maintained the integrity of the mortise and the stability of the talus. Controversy remains about the treatment of deltoid ligament injuries. Many authors advocate an operative repair for deltoid ligament ruptures for optimal reduction of lateral malleolar fracture. However, according to recent cadaveric studies and many satisfactory results of clinical studies, excellent results have been reported regarding the ankle joint stability by anatomical reduction of the lateral structure, but only without surgical repair of the medial structure. Fourteen patients with lateral malleolar fractures with associated deltoid ligament injuries treated at Sun General Hospital between January 1990 and June 1995. There were examined clinically and radiologically. We concluded that deltoid ligament repairs should be considered unnecessary as long as fibular fracture are stabilized anatomically with normal medial joint space. However, in cases with higher fracture levels of lateral malleolus, associated with syndesmotic injury, we recommend syndesmotic screw fixation or deltoid ligament repair.
Ankle ; Ankle Injuries ; Ankle Joint ; Cadaver ; Fibula* ; Hospitals, General ; Humans ; Joints ; Ligaments* ; Rupture ; Solar System ; Talus

BACKGROUND: Systemic hypertension produces varying degree of LVH which is associated with increased cardiovascular morbidiity. Previous studies have documented regression of LVH with various antihypertensives including calcium channel blockers, except diuretics and vasodilators. Recently echocadiographic assessment of the change of left ventricular mass(LVM) after antihyertensive therapy have been reported to offer prognostic cardiovascular information. The aim of this echocardiographic study is determining the influence of nicardipine, a calcium channel blocker, on the change of LVM in patients with essential hypertenison. METHODS: Left ventricular mass(LVM) and left ventricular mass index(LVMI) were measured by M-mode echocardiography in 15 patients with essential hypertension. Nicardipine, a calcium channel blocker, was administered for 6 months and two echocardiographies were done before and after administering, respectively. RESULTS: In the 15 patients treated for 6 months, systolic and diastolic pressure remained very significantly decreased compared with pressure before before therapy(135+/-15mmHg vs 168+/-26mmHg, and 86+/-7mmHg vs 105+/-16mmHg, both p<0.01). Concomitantly both LVM and LVMI decreased significantly(209+/-49g vs 235+/-71g, and 116+/-6g/m2 vs 131+/-38g/m2,both p<0.05). And no change was noted in left ventricular cavity size, demonstration that LVM reduction was due to regression of hypertrophy. CONCLUSION: This study showed that nicardipine produced a significant decrease in blood pressure, LVM, and LVMI over the 6 months period. And large and longterm controlled studies are needed for the clarification of the association between nicardipine and regression of LVH in hypertensive patients.
Antihypertensive Agents ; Blood Pressure ; Calcium Channel Blockers ; Calcium Channels ; Diuretics ; Echocardiography ; Humans ; Hypertension ; Hypertrophy ; Nicardipine* ; Vasodilator Agents

The imprinted tumour suppressor NOEY2 is downregulated in various cancer types, including ovarian cancers. Recent data suggest that NOEY2 plays an essential role in regulating the cell cycle, angiogenesis and autophagy in tumorigenesis. However, its detailed molecular function and mechanisms in ovarian tumours remain unclear. In this report, we initially demonstrated the inhibitory effect of NOEY2 on tumour growth by utilising a xenograft tumour model. NOEY2 attenuated the cell growth approximately fourfold and significantly reduced tumour vascularity. NOEY2 inhibited the phosphorylation of the signalling components downstream of phosphatidylinositol-3’-kinase (PI3K), including phosphoinositide-dependent protein kinase 1 (PDK-1), tuberous sclerosis complex 2 (TSC-2) and p70 ribosomal protein S6 kinase (p70S6K), during ovarian tumour progression via direct binding to vascular endothelial growth factor receptor-2 (VEGFR-2). Particularly, the N-terminal domain of NOEY2 (NOEY2-N) had a potent anti-angiogenic activity and dramatically downregulated VEGF and hypoxia-inducible factor-1α (HIF-1α), key regulators of angiogenesis. Since no X-ray or nuclear magnetic resonance structures is available for NOEY2, we constructed the threedimensional structure of this protein via molecular modelling methods, such as homology modelling and molecular dynamic simulations. Thereby, Lys15 and Arg16 appeared as key residues in the N-terminal domain. We also found that NOEY2-N acts as a potent inhibitor of tumorigenesis and angiogenesis. These findings provide convincing evidence that NOEY2-N regulates endothelial cell function and angiogenesis by interrupting the VEGFR-2/PDK-1/GSK-3β signal transduction and thus strongly suggest that NOEY2-N might serve as a novel anti-tumour and anti-angiogenic agent against many diseases, including ovarian cancer.

The imprinted tumour suppressor NOEY2 is downregulated in various cancer types, including ovarian cancers. Recent data suggest that NOEY2 plays an essential role in regulating the cell cycle, angiogenesis and autophagy in tumorigenesis. However, its detailed molecular function and mechanisms in ovarian tumours remain unclear. In this report, we initially demonstrated the inhibitory effect of NOEY2 on tumour growth by utilising a xenograft tumour model. NOEY2 attenuated the cell growth approximately fourfold and significantly reduced tumour vascularity. NOEY2 inhibited the phosphorylation of the signalling components downstream of phosphatidylinositol-3’-kinase (PI3K), including phosphoinositide-dependent protein kinase 1 (PDK-1), tuberous sclerosis complex 2 (TSC-2) and p70 ribosomal protein S6 kinase (p70S6K), during ovarian tumour progression via direct binding to vascular endothelial growth factor receptor-2 (VEGFR-2). Particularly, the N-terminal domain of NOEY2 (NOEY2-N) had a potent anti-angiogenic activity and dramatically downregulated VEGF and hypoxia-inducible factor-1α (HIF-1α), key regulators of angiogenesis. Since no X-ray or nuclear magnetic resonance structures is available for NOEY2, we constructed the threedimensional structure of this protein via molecular modelling methods, such as homology modelling and molecular dynamic simulations. Thereby, Lys15 and Arg16 appeared as key residues in the N-terminal domain. We also found that NOEY2-N acts as a potent inhibitor of tumorigenesis and angiogenesis. These findings provide convincing evidence that NOEY2-N regulates endothelial cell function and angiogenesis by interrupting the VEGFR-2/PDK-1/GSK-3β signal transduction and thus strongly suggest that NOEY2-N might serve as a novel anti-tumour and anti-angiogenic agent against many diseases, including ovarian cancer.

The human papillomavirus (HPV)-18 E7 (E7) oncoprotein is a major transforming protein that is thought to be involved in the development of cervical cancer. It is well-known that E7 stimulates tumour development by inactivating pRb. However, this alone cannot explain the various characteristics acquired by HPV infection. Therefore, we examined other molecules that could help explain the acquired cancer properties during E7-induced cancer development. Using the yeast two-hybrid (Y2H) method, we found that the Elk-1 factor, which is crucial for cell proliferation, invasion, cell survival, anti-apoptotic activity, and cancer development, binds to the E7. By determining which part of E7 binds to which domain of Elk-1 using the Y2H method, it was found that CR2 and CR3 of the E7 and parts 1–206, including the ETS-DNA domain of Elk-1, interact with each other. As a result of their interaction, the transcriptional activity of Elk-1 was increased, thereby increasing the expression of target genes EGR-1, c-fos, and E2F. Additionally, the colony forming assay revealed that overexpression of Elk-1 and E7 promotes C33A cell proliferation. We expect that the discovery of a novel E7 function as an Elk-1 activator could help explain whether the E7 has novel oncogenic activities in addition to p53 inactivation. We also expect that it will offer new methods for developing improved strategies for cervical cancer treatment.

Translationally controlled tumor protein (TCTP) is a regulatory protein that plays pivotal roles in cellular processes including the cell cycle, apoptosis, microtubule stabilization, embryo development, stress responses, and cancer. However, the molecular mechanism by which it promotes tumor angiogenesis is still unclear. In this study, we explored the mechanisms underlying stimulation of angiogenesis by a novel TCTP. Recombinant TCTP enhanced vascular endothelial growth factor (VEGF)-induced endothelial cell migration, capillary-like tubular structure formation, and cell proliferation by interacting with VEGF receptor 2 (VEGFR-2) in vitro. In contrast, we showed that TCTP knockdown (using short interfering [si]TCTP) led to a decrease in ovarian tumor cells. We also examined the expression of VEGF and hypoxia inducible factor 1 (HIF-1α), an important angiogenic factor.The expression of VEGF as well as HIF-1α was dramatically decreased by siTCTP. Mechanistically, siTCTP inhibited VEGFR-2 tyrosine phosphorylation and phosphorylation of its downstream targets PI3K, Akt, and mTOR. Collectively, these findings indicate that TCTP can promote proliferation and angiogenesis via the VEGFR-2/PI3K and mTOR signaling pathways in ovarian tumor cells, providing new insight into the mechanism behind the involvement of TCTP in tumor angiogenesis.

Translationally controlled tumor protein (TCTP) is a regulatory protein that plays pivotal roles in cellular processes including the cell cycle, apoptosis, microtubule stabilization, embryo development, stress responses, and cancer. However, the molecular mechanism by which it promotes tumor angiogenesis is still unclear. In this study, we explored the mechanisms underlying stimulation of angiogenesis by a novel TCTP. Recombinant TCTP enhanced vascular endothelial growth factor (VEGF)-induced endothelial cell migration, capillary-like tubular structure formation, and cell proliferation by interacting with VEGF receptor 2 (VEGFR-2) in vitro. In contrast, we showed that TCTP knockdown (using short interfering [si]TCTP) led to a decrease in ovarian tumor cells. We also examined the expression of VEGF and hypoxia inducible factor 1 (HIF-1α), an important angiogenic factor.The expression of VEGF as well as HIF-1α was dramatically decreased by siTCTP. Mechanistically, siTCTP inhibited VEGFR-2 tyrosine phosphorylation and phosphorylation of its downstream targets PI3K, Akt, and mTOR. Collectively, these findings indicate that TCTP can promote proliferation and angiogenesis via the VEGFR-2/PI3K and mTOR signaling pathways in ovarian tumor cells, providing new insight into the mechanism behind the involvement of TCTP in tumor angiogenesis.

Translationally controlled tumor protein (TCTP) is a regulatory protein that plays pivotal roles in cellular processes including the cell cycle, apoptosis, microtubule stabilization, embryo development, stress responses, and cancer. However, the molecular mechanism by which it promotes tumor angiogenesis is still unclear. In this study, we explored the mechanisms underlying stimulation of angiogenesis by a novel TCTP. Recombinant TCTP enhanced vascular endothelial growth factor (VEGF)-induced endothelial cell migration, capillary-like tubular structure formation, and cell proliferation by interacting with VEGF receptor 2 (VEGFR-2) in vitro. In contrast, we showed that TCTP knockdown (using short interfering [si]TCTP) led to a decrease in ovarian tumor cells. We also examined the expression of VEGF and hypoxia inducible factor 1 (HIF-1α), an important angiogenic factor.The expression of VEGF as well as HIF-1α was dramatically decreased by siTCTP. Mechanistically, siTCTP inhibited VEGFR-2 tyrosine phosphorylation and phosphorylation of its downstream targets PI3K, Akt, and mTOR. Collectively, these findings indicate that TCTP can promote proliferation and angiogenesis via the VEGFR-2/PI3K and mTOR signaling pathways in ovarian tumor cells, providing new insight into the mechanism behind the involvement of TCTP in tumor angiogenesis.