No abstract available.
Genes, ras* ; Humans*

In order to investigate the validity of the Steel's gluteus medius and minimus advancement, we reviewed 21 hips in 14 spastic cerebral palsy patients, who had advancement of the gluteus medius and minimus insertion for the correction of in-toeing gait between November 1985 and February 1992. The procedure was limited to those patients who had moderate to severe in-toeing gait with positive Steel's stretch reflex. There were eight boys and six girls. The average age at the time of surgery was 6.7 years(2.9 years-11.9 years). The procedure was performed on both hips in seven patients. Of the 14 patients, nine had diplegia, three hemiplegia, and two paraplegia. The average follow-up time was 4.3 years(1 year-8.5 years). In-toeing gait was converted to neutral or physiologic out-toeing gait in 17 hips(81%), excessive out-toeing in 2 cases(9.5%), and mild residual in-toeing in 2 cases(9.5%), Steel's stretch reflex, which was present in all cases preoperatively, disappered in 19 hips(90.5%) postoperatively, Abductor power, however, decreased from 4+ to 4− in average postoperatively, Among the 16 hips, which had no Trendelenburg sign or gait preoperatively, 8 hips(50%) showed positive Trendelenburg sign and gait postoperatively. In conclusion, Steel's gluteus medius and minimus advancement appears to be effective in the correction of in-toeing gait, but there is high risk of weakening the abductor power.
Cerebral Palsy ; Female ; Follow-Up Studies ; Gait ; Hemiplegia ; Hip ; Humans ; Muscle Spasticity ; Paraplegia ; Reflex, Stretch

A case of papillary ependymoma in the left frontal lobe was presented, because in Korea the cerebral ependymoma with noattachment to the ventricles was very rare. The patient was 40 years old female who had complained of severe headache and experienced occasional generalized tonic convulsions for 2 years prior to admission. We could treat the patient successfully by surgery. The tumor mass was attached to a part of the wall of a large cystic cavity which located within the brain substance of left frontal lobe. The tumor tissue was soft and papillary, and looked like a choroid plexus in the ventricles or a mural nodule in the wall of a large cyst which we may find occasionally in cerebellar hemangioblastomas. The cyst was filled with clear limpid yellow fluid of about 120cc. The cyst-wall was not lined with any membrane, and was devoid of tumor tissue. The microscopic findings of tumor showed many papillary growths with the stroma having telangiectasias and irregular mixture of fibrous connective tissue and neuroglial cells.
Adult ; Brain ; Choroid Plexus ; Connective Tissue ; Ependymoma* ; Female ; Frontal Lobe* ; Headache ; Hemangioblastoma ; Humans ; Korea ; Membranes ; Neuroglia ; Seizures ; Telangiectasis

This study aimed to evaluate whether the elevated level of hypoxia-inducible factor-1 alpha (HIF-1 alpha) correlated with histologic types, angiogenesis, tumor cell proliferation, and clinical parameters in common non-small cell lung carcinomas (NSCLCs). We performed immunohistochemical stains using paraffin-embedded tissue blocks from 84 cases of operable NSCLC [No. of squamous cell carcinoma (SCC), 45; No. of adenocarcinoma (AC), 39]. HIF-1 alpha expression was related with histologic types (66.7% in SCCs vs 20.5% in ACs, p<0.001), but not with lymph node status, tumor stage, vascular endothelial growth factor expression, microvessel density (MVD), and proliferating cell nuclear antigen (PCNA) index (p>0.05, respectively). As for the histologic types, MVD and PCNA index were significantly higher in SCCs than in ACs (p=0.009 and p=0.016, respectively). Among HIF-1 alpha positive carcinomas, MVD was significantly higher in HIF-1 alpha positive SCCs than in HIF-1 alpha positive ACs (p=0.023). The overall survival curves were not associated with HIF-1 alpha expression or any other histologic parameters (p>0.05). These findings suggest that HIF-1 alpha expression in NSCLCs may play a differential role according to histologic types, but its prognostic significance is indeterminate.
Adenocarcinoma/metabolism* ; Adenocarcinoma/pathology ; Animals ; Antigens, CD34/metabolism ; Carcinoma, Non-Small-Cell Lung/metabolism* ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Non-Small-Cell Lung/surgery ; Carcinoma, Squamous Cell/metabolism* ; Carcinoma, Squamous Cell/pathology ; Cell Division/physiology* ; Human ; Immunohistochemistry ; Proliferating Cell Nuclear Antigen/metabolism ; Survival Rate ; Transcription Factors/metabolism* ; Vascular Endothelial Growth Factor A/metabolism

Objectives: Coronary heart disease (CHD) risk increases in women after menopause, but menopausal hormone therapy (MHT) helps prevent CHD if started early after menopause. To explore the mechanism underlying the direct vascular actions of estrogen, the effects of 17β-estradiol (E2) on apoptosis of vascular smooth muscle cells (VSMCs) induced with lysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoprotein, were investigated in the present study. Methods: VSMCs were isolated from rat aortas. Apoptosis and protein expression of caspases were assessed using propidium iodide staining and Western blot analysis, respectively. Intracellular formation of reactive oxygen species (ROS) was examined using dichlorofluorescein diacetate, a cell-permeable oxidation-sensitive probe, and quantitated with flow cytometry. Nuclear factor-κB (NF-κB) activation was determined after transfection with a reporter plasmid containing the luciferase reporter gene. Results: After pre-treatment for 24 hours, 17β-E2 suppressed lysoPC-induced (15 mM) apoptotic cell death in a dose-dependent manner with statistical significance at near physiological concentration. 17β-E2 (10−6 M) also increased protein levels of caspase-9 and -8 precursors and decreased the active form of caspase-3. Western blot analysis using subcellular fractions showed that 17β-E2 decreased mitochondrial Bax levels and concomitantly increased cytosolic Bax expression. Furthermore, intracellular production of ROS and NF- κB-mediated transcriptional activity were reduced with 17β-E2. In addition, estrogen effects on apoptosis were partially blocked by ICI 182,780, a specific estrogen receptor antagonist. Conclusions In cultured VSMCs treated with lysoPC, 17β-E2 reduced apoptotic cell death by down-regulating both extrinsic and intrinsic apoptosis pathways, contributing to the preventive action of MHT against CHD.

Objectives: When administered soon after menopause, hormone therapy can prevent coronary heart diseases in women. To explore the mechanism underlying the cardioprotective actions of estrogen, we investigated the effects of 17β-estradiol (17β-E2) on the plasminogen activator system using cultured vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from rat aortas. Protein expression of plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (t-PA) were evaluated using Western blotting and enzyme-linked immunosorbent assay, respectively. The enzyme activity of PAI-1 in a conditioned medium was assessed via reverse fibrin overlay zymography and that of t-PA was assessed via fibrin overlay zymography. Gene expression was quantified using real-time reverse transcription-polymerase chain reaction. Results: Following pre-treatment for 24 hours, 17β-E2 suppressed both protein expression and enzyme activity of PAI-1 stimulated by lysophosphatidylcholine (lysoPC) in a significant and dose-dependent manner at a near physiological concentration. Moreover, 17β-E2 (10−7 M) inhibited PAI-1 gene expression, and ICI 182,780—a specific estrogen receptor antagonist—blocked the effects of 17β-E2 on the PAI-1 protein. 17β-E2 did not affect t-PA secretion but significantly enhanced free t-PA activity through reduced binding to PAI-1. Furthermore, 17β-E2 suppressed intracellular reactive oxygen species production and nuclear factor-κB-mediated transcription. Conclusions In VSMCs stimulated with lysoPC, 17β-E2 reduced PAI-1 expression through a non-receptor-mediated mechanism via antioxidant activity as well as a receptor-mediated mechanism; however, it did not alter t-PA secretion. Of note, 17β-E2 suppressed PAI- 1 activity and concurrently enhanced t-PA activity, suggesting a beneficial influence on fibrinolysis.

PURPOSE: To assess the toxicity and tumor response induced by DCVac/IR(R) dendritic cell (DC) immunotherapy combined with irradiation for refractory colorectal cancer patients with multiple liver metastases. MATERIALS AND METHODS: Between May 2004 and November 2006, applicants from a pool of refractory colorectal cancer patients with multiple liver metastases were enrolled. The patients were registered after having signed the informed consent form, which had been approved by the Institutional Review Board from the Dong-A University and Busan National University Hospital. DCs were obtained from peripheral blood of each patient, and then cultured in vitro. A total of 6x10(6) DCs were packed into a vial (DCVac/IR(R), 0.5 ml) at the convenience of each patient's schedule. On the day before and on the day of each vaccination, each patient received a 4 Gy radiation dose to the target tumor. On the day of vaccination, the indicated dose of autologous DCs was injected into the irradiated tumor using ultrasound-guided needle injection procedures. A total of four vaccinations were scheduled at three 2-week intervals and one 4 week interval at the Dong-A University and Busan National University Hospital. If the tumor status was deemed to be stable or responding to therapy, an additional vaccination dose or two was approved at 4 week intervals beyond the fourth immunization. A tolerance test for DCs was conducted by injecting a range of doses (3x10(6) to 12x10(6) DCs) after the 3rd injection. Moreover, the maximal tolerable dose was applied to additional patients. Treatment safety was evaluated in all patients who had at least one injection. Treatment feasibility was evaluated by the 10th week by assessing the response of patients having at least 4 injections. For systemic toxicities, the evaluation was performed using the National Cancer Institute Common Toxicity Criteria, whereas adverse effects were recorded using common WHO toxicity criteria. RESULTS: Of the 24 registered patients, 22 received the DCs injections. Moreover, of the 14 patients that applied for the tolerance test, only 11 patients completed it because 3 patients withdrew their testing agreement. A grade 3 or more side effect, which was possibly related to the DC injection, did not occur in additional patients. The 12x10(6) DC injection was identified as the maximum tolerable dose, and was then injected in an additional 8 patients. Patients tolerated the injection fairly well, with no fatal side effects. In order to assess the feasibility of DC immunotherapy, the response was evaluated in other hepatic lesions outside of the targeted hepatic lesion. The response evaluation was performed in 15 of the 17 patients who received at least 4 injections. Stable and progressive disease was found in 4 and 11 patients, respectively. CONCLUSION: The DC-based immunotherapy and radiotherapy is theoretically synergistic for the local control and systemic control. The DCVac/IR(R) immunotherapy combined with irradiation was tolerable and safe in the evaluated cases of refractory colorectal cancer with multiple liver metastases. Future work should include well designed a phase II clinical trials.
Appointments and Schedules ; Colorectal Neoplasms ; Consent Forms ; Dendritic Cells ; Ethics Committees, Research ; Humans ; Immunization ; Immunotherapy ; Liver ; National Cancer Institute (U.S.) ; Needles ; Neoplasm Metastasis ; Radiation Dosage ; Vaccination

BACKGROUND: The multidrug resistance (mdr1), multidrug resistance associated protein (mrp1), and glutathione-s-transferase (gst) pi genes have been associated with treatment failure in acute myeloid leukemia (AML). c-jun N-terminal kinase (JNK) activity is increased in response to chemotherapeutic agent. METHODS: To investigate the significance of multidrug resistance (mdr) parameters and JNK activity, bone marrow or peripheral blood cells from 52 patients with AML were analyzed. RT-PCR was performed for mdr1, mrp1, and gst pi gene expression. JNK expression and activity were measured using an immunoe- nzymatic kinase assay and a western blot method. RESULTS: High level expression of mdr1, mrp1, and gst pi mRNA was observed in 38.5%, 48.1% and 54.3% of AML cases, respectively. The remission rate was significantly low in cases with an older age (>55 yr), a high WBC count, poor chromosomal abnormalities, a high level expression of mdr1 and mrp1. The WBC count and mdr1 mRNA expression were independent predictors for the outcome to induction chemotherapy. There was a shorter duration of overall survival in the patients with an older age, a high WBC count, chromosome aberrations, high level expressions of mdr1 and mrp1 mRNA, and JNK activation. The patient's age, WBC count and chromosomal abnormalities were independent predictors for overall survivals. The majority (28/30) of AML cases did not show any levels of JNK activation except for two cases, which were associated with an extremely high WBC count, chromosomal aberration, high level expressions of mdr1, mrp1 and gst pi mRNA, and treatment resistance. CONCLUSIONS: These data indicate the influences of mdr1 and mrp1 mRNA expression on the clinical outcome of AML to induction chemotherapy. But it will be necessary to investigate further whether blast cells of AML resistant to chemotherapy retain the capacity to activate JNK, and relate to MDR parameters.
Adolescent ; Adult ; Aged ; *Drug Resistance, Multiple/genetics ; *Drug Resistance, Neoplasm/genetics ; Female ; Glutathione S-Transferase pi/genetics ; Humans ; JNK Mitogen-Activated Protein Kinases/*metabolism ; Leukemia, Myeloid, Acute/*drug therapy/genetics/metabolism ; Male ; Middle Aged ; Multidrug Resistance-Associated Proteins/genetics ; P-Glycoprotein/genetics ; RNA, Messenger/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Survival Analysis ; Treatment Outcome

Emery-Dreifuss muscular dystrophy is characterized by 1) early contractures of the elbows, Achilles tendons, and postcervical muscles, 2) slowly progressive muscle wasting and weakness with a humeroperoneal distribution in the early stages, and 3) cardiomyopathy with conduction defects and risk of sudden death. The inheritance is usually X-linked recessive but can be autosomal dominant and recessive. We report a case of 28-year old woman who presented with dizziness, palpitation, and progressive muscular weakness. Her ECG revealed high degree AV block and muscle biopsy demonstrated diffuse degenerative change consistent with Emery-Dreifuss muscular dystrophy. She was diagnosed as autosomal dominant Emery-Dreifuss muscular dystrophy by characteristic clinical features, and findings of ECG, nerve conduction test, electromyography and muscle biopsy findings. A VVI-type permanent pacemaker was implanted.
Achilles Tendon ; Adult ; Atrioventricular Block* ; Biopsy ; Cardiomyopathies ; Contracture ; Death, Sudden ; Dizziness ; Elbow ; Electrocardiography ; Electromyography ; Female ; Humans ; Muscle Weakness ; Muscles ; Muscular Dystrophy, Emery-Dreifuss* ; Neural Conduction ; Wills

BACKGOUND: Platelet-derived growth factor (PDGF) is a widely expressed growth factor with both mitogenic and chemotactic activities in many connective tissue cell types. There are four members of PDGF family; PDGF-A, PDGF-B, PDGF-C, PDGF-D. Their biological effects are mediated via two tyrosine kinase receptors, PDGF receptor-alpha and PDGF receptor-beta, and PDGF-mediated signaling is critical for development of many organ systems and acquired disease. The aims of this study were to determine the changes of PDGF-A, PDGF-C and PDGF receptor (PDGFR)-alpha expression in ischemia reperfusion acute renal failure model. METHODS: We examined the expression and localization of PDGF-A, PDGF-C and PDGF receptor-alpha protein using Western blot analysis and immunohistochemistry and PDGF-C mRNA using RNase protection assay after ischemia reperfusion renal failure model. RESULTS: PDGF-A expression showed no change after ischemia reperfusion injury. Proliferating cell nuclear antigen expression increased at day 2 after ischemia reperfusion injury. PDGF-C expression increased at day 2 after ischemia reperfusion injury, and was localized in tubular epithelial cells of outer medulla. PDGFR-alpha increased at day 2 after ischemia reperfusion injury, and was localized in tubular interstitium of outer medulla. CONCLUSION: These results indicated that PDGF-C and PDGF receptor-alpha may have an important role in the renal regeneration after ischemia reperfusion renal injury.
Acute Kidney Injury ; Blood Platelets* ; Blotting, Western ; Connective Tissue Cells ; Epithelial Cells ; Humans ; Immunohistochemistry ; Ischemia* ; Platelet-Derived Growth Factor* ; Proliferating Cell Nuclear Antigen ; Receptor Protein-Tyrosine Kinases ; Receptors, Platelet-Derived Growth Factor ; Regeneration ; Renal Insufficiency* ; Reperfusion Injury ; Reperfusion* ; Ribonucleases ; RNA, Messenger