No abstract available.
Cleft Lip* ; Congenital Abnormalities* ; Skin*

No abstract available.
Animals ; Dogs* ; Facial Bones* ; Periosteum* ; Silicone Elastomers* ; Transplants*

Fluid resuscitation is a basic treatment in hemorrhagic shock. We compared the circulatory responses to fluid resuscitation of 10% pentastarch with those of fresh whole blood and plasmanate in hemorrhagic shock. Eighteen mongrel dogs were bled 24 ml/kg and replaced by equivalent amounts of fresh whole blood(n=6, group B), pentastarch(n=6, group P) and plasmanate(n=6, group PL). Hemodynamic measurements and calculations were performed before and after bleeding and after volume therapy. The decrease of hematocrit and platelet count after volume replacement indicate that hemodilutional effect was maximum 30 min after volume therapy and significantly greater in group P than PL(p<0.05). Central venous pressure(CVP), pulmonary capillary wedge pressure(PCWP) and cardiac index(CI) were increased to 146-189%, 146-172% and 146-175% in group P, respectively during 60 min. These changes were significantly greater than group B and PL(p<0.05). There was delayed recovery of mean arterial pressure in group PL(92% 30 min after volume therapy) compared with group B and P(92% and 93% 5 min). Also group P and PL showed significant prolongation in prothrombin time and partial thromboplastin time during experiment(120 min) and these were significantly more prolonged in group P than PL(P<0.05). And group P showed similar O transport and O extraction ratio to those of group B. The increases in plasma catecholamine were observed after hemorrhage, but no significant changes 5 and 30 min after volume therapy. This suggests that the neurohumoral response to hemodilution was not marked. Mixed venous O2 saturation(SvO2) was directly proportional to CI during experiment(r=0.69, p<0.01), indicating that SvO2 can represent CI during shock and volume therapy. In conclusion, l0% pentastarch is useful as a substitute for fresh whole blood or plasmanate.
Animals ; Arterial Pressure ; Blood Transfusion, Autologous* ; Capillaries ; Dogs* ; Hematocrit ; Hemodilution ; Hemodynamics ; Hemorrhage ; Hydroxyethyl Starch Derivatives ; Partial Thromboplastin Time ; Plasma ; Platelet Count ; Prothrombin Time ; Resuscitation* ; Shock ; Shock, Hemorrhagic*

Ischemic brain hippocampal formation has been developed to understand the relationship between delayed neuronal damage and the expression of NMDA receptor subunits[NR2A, NR2B], MAP2, and NF200 in ttle conditions of hypoxia. Changes of NR subunits[NR2A, 2B], MAP2 6nd NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by morphological change, cytoskeletal disruption was examined through H & E, toluidine blue and immunohistochemical studies. The expression of NR2B was increased than normal at 30 hours after hypoxia. At this time, the expression of MAP2 and NF200 was markedly decreased and their morphology was more eosinophilic than normal and then became darker with expanded perineuronal space. Irreversible neuronal cell damage in hypoxic hippocampal formation is most prominent in CA3 region of hippocampus and the process is triggered by Ca2+ influx through NR1/MR2B receptor channel at 30 hour after initial hypoxic insult. Ca2+ influx through NR1/MR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which causes neuronal cell death. And, morphological changes of neuronal cells in hypoxic conditions were manifested as red neurons in the stage of reactive change, and as dark neuron in the stage of late hypoxic cell damage.
Animals ; Anoxia* ; Brain ; Cell Death ; Cell Membrane ; Cytoskeleton ; Eosinophils ; Hippocampus* ; N-Methylaspartate ; Neurons ; Peptide Hydrolases ; Proteolysis ; Rats* ; Receptors, N-Methyl-D-Aspartate ; Tolonium Chloride

The expression of nm23-H1, nm23-H2, p53, c-myc, cyclin D1, and k-ras genes were investigated in TCDD transformed human keratinocyte RHEK1 cells by exposure to UVB 200 J/m2. For 3 days after irradiation the transcriptional kinetics of these genes were evaluated. The expression of nm23-H1 and H2 were highly increased at 6 hours post-irradiation and recovered in about 3 days to level of pre-irradiation. In cyclin D1 there was a temporary increased expression at 3 hours post-irradiation, but after that time its expression increased minimally. The kinetic of p53 expression was not constant, but showed a decreased tendency. K-ras expression level was decreased by degrees. The decrease in c-myc expression might be related to wavelength-specific induction. In this experiment, S-phase prolongation was a typical alternation in early phase after UVB irradiation. The decreased p53 and k-ras expression and the increased expression of cyclin D1 pushed G1-epsilonS phase transition, and during prolonged S-phase the increased expression of nm23-H1 and H2 might be involved in cell cycle progression, suggesting a function concomitant with prolongation of S-phase after UVB irradiation. TCDD transformed human keratinocyte RHEK1 cell line had 2 heterogeneous cell clones, near diploid and hypotetraploid, and were more resistant against UVB irradiation than RHEK1 cell line. And it had S-phase prolongation instead of G1 arrest in response to UVB irradiation, which may have negative effect to be accumulated DNA mutation without DNA repair.
Blotting, Northern ; Cell Cycle ; Cell Line ; Clone Cells ; Cyclin D1 ; Diploidy ; DNA ; DNA Repair ; Genes, ras ; Humans* ; Keratinocytes* ; Kinetics ; Phase Transition ; Tetrachlorodibenzodioxin*

Nalbuphine, a recently introduced agonist-antagonist analgesic is considered to have analgesic potency similar to morphine in common clinical doses and has been reported to possess an ceiling effect on respiratory depression and to be effective in reversing respiratory depression induced by oxymorphone or hydromorphone. To evaluate the respiratory depression of nalbuphine hydrochloride, we use displacement of CO2 response by a rebreathing method as the index of respiratory depression. Eight healthy male subjects were given the nalbuphine at a dose of 0.1 mg/kg(nalbuphine group) or same volume of normal saline as a placebo(placebo group) intravenously, at interval of 2 weeks by a double blind test. We measured end-tidal PCO2(PETCO2), minute ventilation (VE), tidal volume(VT), and respiratyory frequency(f) at 10 min, 30 min, 60 min and 90 min after the injection. The linear regression equations of VE in response to PCO2 10 min, 30 min, 60 min and 90 min after injection are y=-11.3+0.34X(R=0.66), y=-11.5+0.3X(R=0.53), y=-9.85+0.33X(R =0.61) and y=-11.8+0.37X(R=0.67) in placebo group and y=-11.1+0.30X(R=0.54), y= 13.1+0.35X(R=0.64), y=-11.3+0.33X(R=0.66) and y=-13.4+0.37X(R=0.63) in nalbuphine group.There were no significant differences in the slope of the CO2 response curves between placebo group and nalbuphine group. But there were rightward displacements of the CO2 response curves, which were significant rightward displacements at 60 min and 90 min after the injection(P<0.05). These findings demonstrate that nalbuphine hydrochloride might be a respiratory depressant.
Healthy Volunteers* ; Humans ; Hydromorphone ; Injections, Intravenous* ; Linear Models ; Male ; Morphine ; Nalbuphine* ; Oxymorphone ; Respiratory Insufficiency ; Ventilation

BACKGROUND: Incorrect infusion of dopamine can be potentially life threatening. If the actual volume of a 100 ml intravenous bag or bottle used to mix dopamine solutions is greater than the labeled volume, overdilution of dopamine can occur, resulting in ineffective hemodynamic response. To determine the significance of dopamine overdilution induced by the excessive volume, dopamine concentration and hemodynamic effect were compared in the manually mixed dopamine and the manufactured premixed dopamine. METHODS: For 5% dextrose water (D5W) 100 ml intravenous bottle mixed with 160 mg (4 ml) of dopamine (group 1), D5W 96 ml mixed with 160 mg of dopamine (group 2), premixed dopamine with 1.6 mg/ml of concentration manufactured 2 months ago (group 3), premixed dopamine with 1.6 mg/ml of concentration manufactured 6 months ago (group 4), and D5W 100 ml intravenous bottle mixed with 160 mg (4 ml) of dopamine after removal of 4 ml dextrose water (group 5), dopamine concentration was measured by High performance liquid chromatography (HPLC). Hemodynamic data was obtained from 10 mongrel dogs for each group at baseline (T1), 15 minutes after dopamine infusion at a rate of 3 microgram/kg/min (T2), 8 microgram/kg/min (T3), and 15 microgram/kg/min (T4). RESULTS: Dopamine concentrations of group 1, 2, 3, 4, and 5 were 1.51+/- 0.09, 1.60 +/- 0.10, 1.63 +/- 0.06, 1.57+/- 0.08 and 1.57+/- 0.07 mg/ml, respectively. Group 1 showed a significantly low concentration (p< 0.05). There was no significant differences in all hemodynamic data between group 1, 2, 3, and 4. In group 1, however, there was no significant increase in both mean blood pressure at T4 and mixed venous oxygen saturation at T3 compared with T1. CONCLUSIONS: The actual volume of D5W in 100 ml intravenous bottle is greater than the labeled, and therefore can cause significant overdilution of dopamine. Premixed dopamine, however, has the same concentration and hemodynamic effects as the dopamine mixed manually but precisely.
Animals ; Blood Pressure ; Chromatography, Liquid ; Dogs ; Dopamine* ; Glucose ; Hemodynamics* ; Oxygen ; Water

BACKGROUND: Pleural eosinophilia is rare and commonly considered to be an indicator of good prognosis. The diagnostic significance of eosinophilic pleural effusions remains controversial despite a century of observation and discussion. This study was conducted to assess the prevalence of eosinophilia in 446 consecutive samples of pleural fluid, to review the cause of eosinophilic pleural effusion and to determine whether the presence of eosinophils increases the likehood of benign conditions. METHOD: A retrospective analysis was performed upon patients that underwent first thoracentesis due to pleural effusion between January 1999 and December 1999. RESULTS: Eosinophilic pleural effusions were identified in 24 of the 446 patients (5.4%). Malignancy, parapneumonic effusion and tuberculosis were determined the major causes of pleural effusion (80.6%). Malignancy was diagnosed as frequently in eosinophilic effusions as in non-eosinophilic effusions (54.2% vs 50.5%, p=0.725). No difference was found in the prevalence of eosinophilic and non-eosinophilic effusion according to the etiology. The mean blood eosinophil ratio in patients with eosinophilic pleural effusion was 5.4% and no significant correlation existed between the blood and pleural eosinophilic count. CONCLUSION: Pleural eosinophilia is not helpful for differentiating benign and malignant etiology and is not related with blood eosinophilia or repeated tapping.
Eosinophilia ; Eosinophils* ; Humans ; Pleural Effusion* ; Prevalence ; Prognosis ; Retrospective Studies ; Tuberculosis

Histopathology of pulmonary lymphangioleiomyomatosis(LAM) is studied using four new cases and six previously reported cases, which include two cases without definite evidence of LAM. The important diagnostic features of this lesion were nodular proliferation of immature smooth muscle and cleft or cyst formation within the nodules of smooth muscle cells. The nuclei of the smooth muscle cells were bigger than those of blood vessels or fibrotic lung, and the direction of nuclei was irregular. The lung parenchyma showed little inflammatory change but there were multiple air cysts with smooth muscle nodules at their margin. There were two cases with exuberant proliferation of smooth muscle nodules and two cases with papilliferous projections of the cells into lymphatic lumen. Whereas, three cases had only a few small slender nodules of smooth muscle cells at the margin of air cyst. The lymphatic lumen with smooth muscle nodules is dilated in four cases but other four cases show collapsed lumen. Pulmonary hemorrhage and hemosiderosis were prominent in three cases. There were variety of histology in terms of the cellularity of smooth muscle nodules, the size of the lymphatic lumen and the degree of pulmonary destruction, which may have significance on the clinical presentation and prognostication.
Cysts

BACKGROUND: The antitumor effects of herpes simplex virus thymidine kinase(HSV-tk) and ganciclovir(GCV) strategies for cancer gene therapy have a the following advantages:1) a direct cytotoxicity to HSV-tk modified cancer cells by GCV 2) a cell death by the local transfer of toxic metabolites from the HSV-tk modified cells to nearby unmodified tumor cells(bystander effect), and 3) in vivo bystander effect such as antitumor-immunity. Retroviral and adenoviral sequences can silence transgene expression in cells and mice. In this study, we investigated the above described advantages of HXV-tk/GCV strategy in Lewis lung cell and mouse lung cancer model using retroviral vector and adenoviral vector. Also, we observed whether the expression of a silenced gene can be reactivated by treating cell with butyrate. METHODS: Retrovirus-HSV-tk and adenovirus-HSV-tk vectors were used for the transduction of Lewis lung carcinoma(LLC) cells. The change of HSV-tk expression by butyrate was measured by Western blot.The antitumor activities containing bystander effect were observed in vivo(by MTT assay) and in vivo tumor models of various combinations of LLC and LLC-tk. RESULTS: 1. Butyrate induced the enhancement of HSV-tk expression from adenovirally transduced cells but not from retrovirally transduced cells. 2. Both retrovirus-HSV-tk and adenovirus-HSV-tk vectors with GCV treatment were effective for killing of tumor cell in vitro and suppression of LLC tumorigenicity. Bystander effect was responsible for killing of mixture of LLC-tk and LLC in vitro and in vivo-tumorigenicity model. CONCLUSION: Butyrate could augment adenoviral vector seems to be an effective approach for lung cancer therapy.
Adenoviridae ; Animals ; Butyrates ; Bystander Effect ; Carcinoma, Lewis Lung* ; Cell Death ; Genes, Neoplasm ; Genetic Therapy* ; Herpes Simplex* ; Homicide ; Lung ; Lung Neoplasms ; Mice* ; Phosphotransferases* ; Retroviridae ; Simplexvirus* ; Thymidine ; Transgenes ; Zidovudine*