No abstract available.

No abstract available.

The incidence of infective endocarditis is 1.5-4.95 cases per 100,000 individuals per year, with a mortality of 14-46% 1-year post infection. The management and decision to operate on selected patients remains controversial. Our study reviews cases of native and prosthetic valve endocarditis in a surgical population, in an attempt to identify and compare clinical and microbiologic features between the two groups. In addition, we compared our findings with other published series to identify if there are changes with these parameters over time.

GTPrS-dependent phospholipase D activity in human neutrophils was investigated using exogenous phospholipid as a substrate. Both cytosolic and membrane- associated phospholipase D activities were identified. The previously described 50 kDa cytosolic activating factor was resolved chromatographically from the cytosolic phospholipase D. Using exogenous phospholipid as substrate along with chromatographically resolved 50 kDa factor and recombinant ADP-ribosylation factor 1, plasma membrane was required for activity, indicating that the activity which was previously seen using endogenous phospholipid substrate was due to a phospholipase D located in the plasma membrane. In addition, ADP-ribosylation factor and the 50 kDa factor activated synergistically. Using neutrophil plasma membranes, a third regulator of neutrophil membrane phospholipase D was identified from bovine brain cytosol. This factor was resolved from ADP-ribosylation factor and Rho A by successive column chromatographies. The brain factor showed a synergistic effect with the 50 kDa neutrophil activator but an additive effect with recombinant ADP- ribosylation factor. Whether or not ADP-ribosylation factor or the brain factor were present, high activities were seen only when the 50 kDa factor was present, indicating that the 50 kDa cytosolic factor is a major activating factor for the neutrophil plasma membrane phospholipase D.
ADP-Ribosylation Factor 1 ; ADP-Ribosylation Factors* ; Brain* ; Cell Membrane ; Chromatography ; Cytosol* ; Fibrinogen ; Humans ; Membranes ; Neutrophils* ; Phospholipase D* ; Phospholipases*

PURPOSE: Antibody mediated rejection (AMR), although less common than acute cellular rejection (ACR), may be recalcitrant to conventional rescue therapy. AMR is caused by de novo B-cell mediated production of immunoglobulin G antibody (IgG) targeted against specific allograft antigen in a presensitized recipient. Rituximab is a chimeric murine- human anti-CD20 monoclonal antibody which targets CD-20 positive B-cells for elimination. Rituximab has been described to improve allograft salvage for refractory AMR. METHODS: From January 2002 to May 2004, 11 patients were diagnosed with AMR. The first 5 patients (non-rituximab group: NRG) were treated with high dose steroids, plasmapheresis followed by IVIG (500 mg/kg/dose) in addition to OKT3 and/or rabbit antithymocyte globulin. The latter 6 patients (rituximab group: RG) were given Rituximab (375 mg/m2) with IVIG following plasmapheresis. All patients had biopsy proven AMR. RESULTS: Four patients received allografts from living donors and one patient from cadaveric donor in NRG. Each three patients received allografts from living or cadaveric donors in RG. One patient of RG had a positive anti-HLA B-cell crossmatch by CDC (complement dependent cytotoxicity). The anti-donor antibody was reduced to zero with negative CDC and flowcytometry through a desensitization protocol prior to transplantation. The time to diagnosis of AMR in both groups were 17.8+/-18.17 days (NRG); 11+/-2.5 days (RG). ACR was identified in conjunction with AMR in 2 (40%: NRG), 4 patients (66.7%: RG), respectively. All patients had biopsies with classic features of AMR on light microscopy, including C4d staining. Three (50%) patients of RG had positive post-transplantation CDC and donor-specific antibody (DSA) identified. Mean serum creatinine (SCr) upon diagnosis of AMR were 4.3+/-1.71 mg/dL (NRG); 5.77+/-2.65 mg/dL (RG). The rescue rate of RG was superior than NRG (83% vs. 40%, P>0.05). The time to rescue from AMR in both groups were 40.5 +/-28.99 days (NRG); 48+/-54.67 days (RG). Mean SCr of the rescued patients were 1.65+/-0.07 mg/dL (NRG); 2.2+/-1.4 (RG) with median follow up of 120 days (range 33~319 days). Allograft nephrectomies were performed in 3 patients of NRG. CONCLUSION: Rescue therapy with Rituximab improves allograft salvage after AMR and should be considered early in the treatment of biopsy proven AMR.
Allografts ; Antilymphocyte Serum ; B-Lymphocytes ; Biopsy ; Cadaver ; Centers for Disease Control and Prevention (U.S.) ; Creatinine ; Diagnosis ; Follow-Up Studies ; Humans ; Immunoglobulin G ; Immunoglobulins, Intravenous ; Kidney Transplantation* ; Kidney* ; Living Donors ; Microscopy ; Muromonab-CD3 ; Nephrectomy ; Plasmapheresis ; Rituximab ; Steroids ; Tissue Donors

urpose: Misonidazole is a radiosensitizer that binds in hypoxic cells. The purpose of this study was to find out the feasibility of I-131-Iodomisonidazole (IMISO) for imaging of tumor hypoxia. MATERIALS AND METHODS: Tosyl precursor was dissolved in acetonitrile and I-131-NaI was added to synthesize IMISO. Balb/c mice inoculated with CT-26 adenocarcinoma were injected with IMISO. Mice were sacrificed at 1,2,4,24 hr and % of injected dose per gram of tissue (%ID/g) was determined. For scintigraphy and MRI, mouse bearing CT-26 adenocarcinoma was administered with IMISO and imaging was performed 4 hr after. Then, mouse body was fixed and microtomized slice was placed on radiographic film for autoradiography. RESULTS: %ID/g of tumor was 1.64 (1h), 0.98 (2h), 0.85 (4h) and 0.20 (24h), respectively. At 24h, %ID/g of tumor was higher than that of all other tissues except thyroid. Tumor to muscle ratio increased with time and tumor to blood ratio also increased with time and reached 1.53 at 24 hr. On autoradiogram, tumor was well visualized as an increased activity in central hypoxic area of the tumor which corresponds to the area of high signal intensity on T2-weighted MR image. On scintigraphy, tumor uptake was visualized. CONCLUSION:: This RESULTS suggest that IMISO may have a potential for tumor hypoxia imaging in mouse model. However, further study is needed to improve it's localization in tumor tissue and to achieve acceptable images of tumor hypoxia.
Adenocarcinoma* ; Animals ; Anoxia* ; Autoradiography ; Magnetic Resonance Imaging ; Mice* ; Misonidazole ; Radionuclide Imaging ; Thyroid Gland ; X-Ray Film

A case of supratentorial ependymoma in a 48-year-old man. After operation and radiological treatment, metastasis to scalp and cervical lymph node occurred, without recurrence of primary focus. 11 cases of intracranial ependymoma with extracranial metastasis were reviewed. Metastasizing intracranial ependymomas are 3 times as frequent in males and originate above tentorium. The most effective transmission of metastasis of ependymoma is through the blood stream and the frequent sites of metastasis are lungs, pulmonary hilus, mediatinum, liver, scalp, vertebra, femoral bone and cervical lymph nodes. Our case is the oldest among reported cases and metastasized to relatively rare site.
Ependymoma* ; Humans ; Liver ; Lung ; Lymph Nodes ; Male ; Middle Aged ; Neoplasm Metastasis* ; Recurrence* ; Rivers ; Scalp ; Spine

Yonsei Cancer Center developed an RF(Radiofrequency) capacitive type heating device, GHT-RF8(Greenytherm) in cooperation with Green Cross Medical Corp., Korea in 1986 for the first time in Korea. Cooperative clinical studies of hyperthermia for the treatment of cancer using GHT-RF8 were conducted by Yonsei Cancer Center in collaboration with the Presbyterian Medical Center, Chonju, Korea. A total of forty patients with various histologically proven malignant tumors, including superficial (N = 13) and deep-seated tumors (N = 27), were treated with this newly developed heating device in conjunction with radiotherapy (N = 38) or chemotherapy (N = 2) at two different institutes between October 1986 and September 1987. These patients were locally far advanced or recurrent cases and considered to be refractory to conventional cancer treatment modalities. Radiotherapy was given in 200cGy per day, five times a week fractionations with a total tumor dose of 50-60Gy in 5-6 weeks. Within an hour after radiotherapy, the RF capacitive type of hyperthermia was given two times a week for a total of 4-10 treatment sessions and an attempt was made to maintain the tumor temperature at 41-45 degrees C for 30-60 minutes. Of forty patients treated, 14 patients with deep-seated tumors showed complete response and 20 patients showed partial response. The overall response rate was 85% (34 out of 40 patients) and only 6 patients showed no response. Complications from this treatment were mainly burns, superficial first degree burn in 2 cases, second degree in 4 cases and subcutaneous fat necrosis was observed in 2 cases.
Adolescent ; Adult ; Aged ; Equipment Design ; Female ; Heating/*instrumentation ; Human ; Hyperthermia, Induced/adverse effects/*instrumentation ; Male ; Middle Age ; Neoplasms/radionuclide imaging/therapy ; Support, Non-U.S. Gov't ; Tomography, X-Ray Computed

No abstract available.
Anesthesia* ; Dexmedetomidine* ; Lidocaine* ; Spine*

Phospholipase D (PLD) is an enzyme involved in signal transduction and widely distributed in mammalian cells. The signal transduction pathways and role for phospholipid metabolism during hormonal response in cortical collecting duct remain partly undefined. It has been reported that dexamethasone increases transepithelial transport in M-1 cells that are derived from the mouse cortical collecting duct. We investigated the expression and activity of PLD in M-1 cells. Basal PLD activity of M-1 cells cultured in the presence of dexamethasone (5 microM) was higher than in the absence of dexamethasone. Dexamethasone and ATP activated PLD in M-1 cells but phorbol ester did not stimulate PLD activity. Vasopressin, bradykinin, dibutyryl cyclic AMP, and ionomycin were ineffective in activating PLD of the cells. The PLD2 isotype was detected by immunoprecipitation but PLD1 was not detected in M-1 cells. Addition of GTPgammaS and ADP-ribosylation factor or phosphatidylinositiol 4,5-bisphosphate to digitonin-permeabilized cells did not augment PLD activity. In intact cells PLD activity was increased by sodium oleate but there was no significant change between dexamethasone treated- and untreated cells by oleate. These results suggest that at least two types of PLD are present in M-1 cells and PLD plays a role in the corticosteroid-mediated response of cortical collecting duct cells.
Animal ; Biological Transport/drug effects ; Dexamethasone/pharmacology* ; Dose-Response Relationship, Drug ; Drug Interactions ; Glycerophospholipids/analysis ; Isoenzymes/drug effects ; Kidney Cortex/cytology ; Kidney Tubules, Collecting/drug effects* ; Kidney Tubules, Collecting/cytology ; Mice ; Mice, Transgenic ; Oleic Acid/pharmacology ; Phospholipase D/drug effects*