OBJECTIVES: The purpose of this study was to get help in order to diagnose orthopaedic disease, measure its activity and determine treatment plan by measuring the beta-glucuronidase activity in urine, serum and joint fluid. METHODS: The beta-glucuronidase activity was determined in the serum, urine and joint fluid of the patients with degenerative arthritis, rheumatoid arthritis, osteomyelitis and osteogenic sarcoma, and some other disease to study the change of the enzyme activity. These values of each specimen were calculated by standard curve and treated by statistical analysis. RESULTS: The results obtained were summarized as follows. 1. The beta-glucuronidase activity in the serum, urine and joint fluid was increased in patients with degenerative arthritis, rheumatoid arthritis, osteomyelitis and osteogenic sarcoma etc. 2. The increased beta-glucuronidase activity in the serum and joint fluid of each disease does not show a specific finding about respective disease, but the increased beta-glucuronidase activity was statistically significant in the urine of all disease groups(male:p=0. 0041, female:p=0. 0001). CONCLUSIONS: On the basis of these results, it was suggested that beta-glucuronidase activity was affected by the orthopaedic disease and differed according to each specimen.
Arthritis, Rheumatoid ; Glucuronidase* ; Humans ; Joints ; Osteoarthritis ; Osteomyelitis ; Osteosarcoma

BACKGROUND: Aside from its well known peripheral antihypertensive effects, calcium also lowers blood pressure, when administered into the cerebral ventricle. The present study was aimed to determine whether the central depressor response to calcium is mediated by a stimulation of endogenous L-arginine-nitric oxide (NO) pathway. METHODA: Mean arterial pressure (MAP) and heart rate (HR) were continuously recorded from the femoral artery in anesthetized rats. Administration of calcium was performed into the right lateral cerebral ventricle. The effects of N G-nitro-L-arginine methyl ester (L-NAME) on the cardiovascular response to calcium were examined. RESULTS: Intracerebroventricular (ICV) injection of calcium consistently produced a decrease in MAP and HR. The depressor and bradycardiac responses to calcium showed a dose-dependent fashion. Pretreatment with a calcium channel blocker, diltiazem (1 micromol, ICV), attenuated cardiovascular responses to calcium. ICV infusion (1 microl/min) of L-NAME (200 microgram/kg and 20 microgram/kg/min for 60 min) increased MAP without significant changes in HR. Chronic ingestion of L-NAME (5 mg/100 ml in drinking water, 4 weeks) also increased the systolic blood pressure as compared with control. The depressor effect of ICV calcium was significantly diminished in acute or chronic L-NAME treated rats. CONCLUSION: These findings suggest that the central depressor response to calcium, at least in part, is NO-dependent.
Animals ; Arterial Pressure ; Blood Pressure ; Calcium Channels ; Calcium* ; Cerebral Ventricles ; Diltiazem ; Drinking Water ; Eating ; Femoral Artery ; Heart Rate ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Rats

BACKGROUND: Calcium plays a key role in vascular contraction and regulates receptor sensitivity to certain neurotransmitters. Calcium channel blockers are useful in the treatment of both clinical and experimental hypertension. The present study was designed to examine whether there is an alteration of the activity of calcium channels in association with the development of hypertension. METHODS: Deoxycorticosterone acetate(DOCA)-salt hypertension was made by subcutaneous implantation of DOCA(200mg/kg)strip plus saline drinking(1%) and 2-kidney, 1 clip(2KIC)hypertension by clipping the left renal artery with a silver clip(internal gap of 0.2mm). They were used 4 weeks later. Age-matched normal rats served as a control. Mean arterial pressure(MAP) and heart rate(HR) were continuously recorded from the right femoral artery. The drugs were administered intravenously. RESULTS: Vehicle alone was without effect on MAP or HR. In normotensive rats, nifedipine infusion(5 and 10ug/kg/min)caused a dose-dependent decrease in MAP without significant changes in HR, while Bay k 8644(Bay K, 5 and 10 ug/kg/min) increased MAP transiently. Both the depressor response to nifedipine and the pressor response to Bay k were more marked in DOCA-salt hypetensive rats than in normotensive rats. The maximal changes in MAP indced by nifedipine(5 and 50 ug/kg) or Bay K(5 and 50 ug/kg) were also enhanced in 2KIC hypertensive rats as compared with control rats. CONCLUSION: These results indicate that calcium channel inhibitors and activators can affect on the regulation of blood pressure in an opposite fashion. It is also suggested that the activity of calcium channels might be altered in the developement of experimental hypertension.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester* ; Animals ; Bays* ; Blood Pressure ; Calcium ; Calcium Channel Blockers ; Calcium Channels ; Desoxycorticosterone ; Femoral Artery ; Heart ; Hypertension ; Neurotransmitter Agents ; Nifedipine* ; Rats* ; Renal Artery ; Silver

Bradykinin has been known to elicit a pressor effect when administered centrally, and a depressor effect when administered peripherally. The present study was aimed at investigating whether the blood pressure response to bradykinin is dependent on the endogenous generation of nitric oxide (NO). Effects of NG-nitro-L-arginine methyl ester (L-NAME) on the pressor and depressor responses to intracerebroventricularly and intravenously injected bradykinin (5nmol/rat), respectively, were examined in anesthetized rats. Neither the pressor response nor the depressor response was affected by acute parenteral treatment with L-NAME. The pressor and depressor effects of bradykinin were also noted in rats chronically supplemented with L-NAME in drinking water for 4 weeks. Bradykinin caused a relaxation of the isolated thoracic aorta in vitro, which was not affected in the presence of L-NAME. However, bradykinin failed to cause a relaxation of the aorta isolated from rats chronically treated with L-NAME. These findings suggest that endogenous generation of NO may not completely account for the blood pressure responses to bradykinin in rats.
Animals ; Aorta ; Aorta, Thoracic ; Blood Pressure* ; Bradykinin* ; Drinking Water ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Rats* ; Relaxation

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 AND OBJECTIVES: The facial nerve grading system proposed by House and Brackmann is the most widely accepted for the clinical assessment of facial nerve injury. It is, however, subjective and discontinuous, and prone to interobserver variation. In order to remove subjectivity from analysis, we have therfore proposed the FEMA grading system at the Korean Otologic Study Group in 1995. This study describes the FEMA grading system and determines its reliability and usefulness by comparing it with the House-Brackmann system in assessing facial paralysis. MATERIALS AND METHODS: Ten experienced otolaryngologists using the FEMA and H-B systems studied 30 patients with various degrees of facial palsy. RESULTS: In the average of coincidence rate, the FEMA system showed 84.4% and the H-B system was 73.7% (p<0.05). The standard deviation in the grading by the FEMA system was lower than that by the H-B system (p=0.082). CONCLUSION: The study found that the FEMA grading system is more exact and objective in describing the severity of facial palsy than the House-Brackmann grading system. Especially, the FEMA grading system is more convenient to use in patients with partial weakness.
Facial Nerve ; Facial Nerve Injuries ; Facial Paralysis ; Humans ; Observer Variation

No abstract available.
Factor VII Deficiency* ; Factor VII*

BACKGROUND: Inflammatory bowel disease (IBD) is an incurable disease that negatively influences the quality of life of patients. Current and emerging therapies target proinflammatory cytokines and/or receptors to downregulate proinflammatory responses, but insufficient remission requires other therapeutic agents. Herein, we report that the synthetic antiinflammatory peptide 15 (SAP15) is capable of cell penetration and anti-inflammatory activity in human macrophages. METHODS: SAP15 was labeled with fluorescence and administered to human leukemia monocytic cells (THP-1) cells for cell penetration analysis. Using biolayer interferometry analysis, the binding affinity of SAP15 with histone deacetylase 5 (HDAC5) was measured. SAP15-treated THP-1 cells were analyzed by protein phosphorylation assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). In addition, in vivo analysis of the therapeutic effect on IBD was observed in a dextran sulfate sodium (DSS)-induced model. Samples from SAP15-treated mice were analyzed at both the macroscopic and microscopic levels using ELISA, myeloperoxidase (MPO) assays, and histological evaluations. RESULTS: SAP15 was internalized within the cytosol and nucleus of THP-1 cells and bound to the HDAC5 protein. SAP15-treated macrophages were assessed for protein phosphorylation and showed inhibited phosphorylation of HDAC5 and other immune-related proteins, which led to increased M2-like macrophage markers and decreased M1-like macrophage markers and tumor necrosis factor-a and interleukin-6 cytokine levels. The SAP15 treatment on IBD model showed significant recovery of colon length. Further histological analysis of colon demonstrated the therapeutic effect of SAP15 on mucosal layer. Moreover, proinflammatory cytokine levels and MPO activity from the plasma show that SAP15 is effective in reduced proinflammatory responses. CONCLUSION These findings suggest that SAP15 is a novel peptide with a novel cell-penetrating peptide with antiinflammatory property that can be used as a therapeutic agent for IBD and other inflammatory diseases.

It is well known that the endothelium plays an important role in the circulation by modulating contractile responses of vascular smooth muscle. This study was designed to investigate the alterations and the mechanisms of endothelial modulation in chronic 2-kidney, 1 clip(2K1C) hypertensive rats. 2K1C hypertension was made by clipping the left renal artery and age-matched control rats received a sham treatment. Aortic rings were mounted in tissue baths for measurement of isometric tension. In rings with endothelium, norepinephrine evoked concentration-dependent contraction. Endothelium removal markedly enhanced the contraction, and the responses were less pronounced in 2K1C rats than control rats. Similar fashion of the contractions by endothelium removal was observed with norepinephrine and the alpha1 drenoceptor agonist phenylephrine in control rats, while phenylephrine did not alter the contraction by endothelium removal in 2K1C rats. The alpha2 drenoceptor agonist clonidine also greatly enhanced the contraction after endothelium removal, however the endothelial inhibition was still shown in 2K1C rats. In contrast to norepinephrine-induced contractions, the enhancement of serotonin-or prostaglandin F2alpha - induced contractions after endothelium removal was small and similar in 2K1C and control rats. NG-nitro-L-arginine methyl ester enhanced the contraction induced by agonists in aortic rings with endothelium, which was similar to the response in rings without endothelium. The relaxation response to acetylcholine was attenuated in 2K1C rats, while the response to sodium nitroprusside remained unaltered. These results indicate the endothelium plays an inhibitory role against contractions in rat aorta by releasing nitric oxide, but the characteristics of the endothelial inhibition are not identical against various agonists. The negative endothelial modulation is more pronounced during alpha1 and alpha2 renoceptor- mediated contractions than during contractions mediated by other receptors. In addition, the inhibitory role of the endothelium against alpha1 drenoceptor agonist-induced contraction is impaired in 2K1C renal hypertension.
Acetylcholine ; Animals ; Aorta ; Baths ; Clonidine ; Dinoprost ; Endothelium ; Hypertension ; Hypertension, Renal ; Muscle, Smooth, Vascular ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitroprusside ; Norepinephrine ; Phenylephrine ; Placebos ; Rats* ; Relaxation ; Renal Artery ; Vasoconstriction*

Trisomy 18 is the second most common chromosomal anomaly that reach to live birth after Down syndrome. Several methods were proposed to screen patients on the risk of Edward syndrome like maternal serum levels using total human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP) and unconjugated estriol (uE3), or free beta hCG with AFP, but the serum screening has only 50-60% detection rate with a 1-2% of false positive rate. So to cover the limitations that serum marker has, detailed ultrasound examination is also necessary and sensitivities of 65-70% were reported. We report a case of trisomy 18 fetus in which second trimester triple markers of maternal serum was normal, but by detailed ultrasound examination, unilateral radius aplasia was diagnosed cytogenetic study confirmed the fetus as trisomy 18.
alpha-Fetoproteins ; Biomarkers ; Chorionic Gonadotropin ; Cytogenetics ; Down Syndrome ; Estriol ; Female ; Fetus ; Humans ; Live Birth ; Mass Screening ; Pregnancy ; Pregnancy Trimester, Second ; Radius* ; Trisomy ; Ultrasonography