Between August 1993 and Apri1 1994, intrarenal arterial color duplex Doppler sonography was performed on 55 patients(110 kidneys) with acute ureteral obstruction and 12 patients(24 kidneys) with painless ureteral obstruction by unilateral ureteral stones to assess renal hemodynamic changes and its clinical applications. The mean resistive index(RI) of the doppler waveforms obtained on the acutely obstructed 55 kidneys(0.663+/-0.055) was significantly higher than that of the contralateral normal kidneys (0.613+/-0.052) (P<0.05). We found no RI difference between the contralateral normal 55 kidneys(mean: 0.613+/-0.052) in patients with acute ureteral obstruction and the painless obstructed 12 kidneys(mean: 0.595+/-0.029). In the acutely obstructed 55 kidneys, the mean RI of the upper pole(0.674+/-0.054) was significantly higher than that of the mid portion(0.661+/-0.064) or the lower pole(0.654+/-0.065,r<0.05). No difference of the RI was found between the hydronephrotic 31 kidneys(mean: 0.671+/-0.063) and nonhydronephrotic 24 kidneys(mean: 0.65+/-0.041) in the acutely obstructed 55 kidneys(P>0.05). There was no correlation between the levels of ureteral obstruction and intrarenal RI values(P>0.05). The RIs of 3 significantly obstructed kidneys decreased after relief of obstruction. We conclude that the RI is easily obtained and measured, and it would provide important physiological informations on renal vascular impedance in acute ureteral obstruction. Renal doppler findings could be the one of the criteria for assessing the upper urinary tract obstruction.
Electric Impedance ; Hemodynamics* ; Humans ; Kidney ; Ultrasonography, Doppler ; Ureter* ; Ureteral Obstruction* ; Urinary Tract

No abstract available.
Child ; Coronary Vessels* ; Echocardiography ; Humans

Bilateral adrenal tuberculosis is a rare disease and often occurs bilaterally. We report a case of bilateral adrenal masses due to tuberculosis with adrenal insufficiency. The patient was a 39- year-old man who had complained of intermittent pain of right upper quadrant and general weakness. The plasma levels of cortisol and catecholamine were normal. The levels of 24-hour urinary catecholamine and VMA were also normal. But the levels of 24-hour urinary 17- hydroxycorticosteroids and 17-ketosteroids were reduced. Abdominal CT showed about 6.5 x4.8 x 5.4cm sized left adrenal mass and 4.0 x 2.8 x 3.6cm sized right adrenal mass with calcification. The result of sono-guided percutaneous needle biopsy was adrenal tuberculosis. The patient was treated with antituberculous chemotherapy and hormonal replacement. But the masses are unchanged during 5-months follow-up.
17-Ketosteroids ; Adrenal Glands ; Adrenal Insufficiency ; Biopsy, Needle ; Drug Therapy ; Follow-Up Studies ; Humans ; Hydrocortisone ; Hydroxycorticosteroids ; Plasma ; Rare Diseases ; Tomography, X-Ray Computed ; Tuberculosis*

STATEMENT OF PROBLEM: Several prosthetic options are available for the restoration of multiple adjacent implants. A passively fitting prosthesis has been considered a prerequisite for the success and maintenance of osseointegration. Passivity is a particular concern with multiple implants because of documented inaccuracies in the casting and soldering process. One way to avoid this problem is to restore the implants individually, however, the restorations of individual adjacent impants requires careful adjustment of interproximal contacts. PURPOSE: The purpose of this study was to compare the stress distribution pattern and amount surrounding Bicon implants with individual crowns and splinted restorations. MATERIAL AND METHOD: A photoelastic model of a human partially edentulous left mandible with 3 Bicon implants(4*1 mm) was fabricated. For non-splinted restorations, individual crowns were fabricated on 3 abutments (4.0*6.5 mm, 0 degree, 2.0 mm post, Bicon Inc., Boston, USA) After the units were cemented, 4 levels of interproximal contact tightness were evaluated: open, ideal (8 micrometershim stock drags without tearing), medium(40 micrometer), and heavy(80 micrometer). Splinted 3-unit fixed partial dentures were fabricated and cemented to the model. Changes in stress distribution under simulated non-loaded and loaded conditions(7.5, 15, 30 lb) were analyzed with a circular polaricope. RESULTS: 1. Stresses were distributed around the entire body of fin in Bicon implants. 2. Splinted restorations were useful for distribution of stress around implants especially with higher loads. 3. By increasing the contact tightness between the individually restored three implants, the stress increased in the coronal portion of implants. CONCLUSIONS: Ideal adjustment of the contact tightness was important to reduce the stresses around individually restored Bicon implants.
Crowns ; Denture, Partial, Fixed* ; Humans ; Mandible ; Osseointegration ; Prostheses and Implants ; Splints

No abstract available.
Byssinosis*

The present study was aimed at investigating the role of type II 11beta-hydroxysteroid dehydrogenase (IIbeta- HSD II) in the development of hypertension. Two-kidney, one-clip (2K1C), deoxycorticosterone acetate (DOCA)/salt, or NG-nitro-L-arginine methyl ester (L-NAME) hypertension was induced in male Sprague- Dawley rats. Four weeks later, the expression of 11beta-HSD II mRNA was determined in the kidney by Northern blot analysis. The plasma level of aldosterone was measured by radioimmunoassay. In 2K1C hypertension, the expression of 11beta-HSD II was decreased in the clipped kidney and increased in the non-clipped kidney. The expression was increased in the remnant kidney of DOCA/salt hypertension, while decreased in the kidneys of L-NAME hypertension. The plasma level of aldosterone was increased, decreased, and remained unchanged in 2K1C, DOCA/salt, and L-NAME hypertension, respectively. The down-regulation of 11beta-HSD II may contribute to the sodium retention, thereby increasing the blood pressure in 2K1C and L-NAME hypertension. On the contrary, the up-regulation in DOCA/salt hypertension may play a compensatory role to dissipate the sodium retention.
11-beta-Hydroxysteroid Dehydrogenases* ; Aldosterone ; Animals ; Blood Pressure ; Blotting, Northern ; Desoxycorticosterone ; Down-Regulation ; Humans ; Hypertension* ; Kidney* ; Male ; NG-Nitroarginine Methyl Ester ; Plasma ; Radioimmunoassay ; Rats* ; RNA, Messenger ; Sodium ; Up-Regulation

BACKGROUND: Ozone (03) induces airway inflammation and hyperresponsiveness which are characteristic features of asthma. There have been few studies observing O3-induced increase in responsiveness of rat airway muscle. Objectives: The aims of this study were to develop an O3-induced nonallergic asthma model using rat tracheal smooth muscle (TSM) and to evaluate the role of airway epithelium on the modulation of muscle responsiveness. METHOD: Five groups of 20 male Sprague-Dawley(SD) rats were exposed to filtered air including 0.12, 0.5, 1.0, or 2.0 ppm 03 for 1 hour. Thirty minutes after the exposure, bronchoalveolar lavage (BAL) and isometric contractile responses of the isolated tracheal ring segments to KCI, acetylcholine (ACh), and electrical field stimulation (EFS) were measured. RESULTS: The percent age of neutrophils was significantly higher and that of alveolar macro-phages in BAL fluid was significantly lower in 2.0 ppm O3-exposed rats than in the control. There were no significant differences in the maximal contractile responses of TSM to KC1, ACh, EFS and in the sensitivity to ACh (ACh-EC50) and EFS (EFS-EC50) between the control group and the ozone exposed group. ACh-EC50 and EFS-EC50 were correlated positively with the percent age of neutrophils and inversely with that of macrophages. Removal of epithelium significantly increased the sensitivity to ACh in O3-exposed group, but not in the control group. CONCLUSION: These findings indicate that O3 induces neutrophilic airway inflammation, but not an increased sensitivity of TSM to ACh or EFS in SD rats. However, O3-induced epithelial damage may be associated with increased muscle response.
Acetylcholine ; Animals ; Asthma ; Bronchoalveolar Lavage ; Epithelium ; Humans ; Inflammation ; Macrophages ; Male ; Muscle, Smooth* ; Neutrophils ; Ozone ; Rats* ; Trachea

No abstract available.
Brain* ; Meningitis* ; Tuberculoma*

OBJECTIVES: Several reports suggest that enhanced generation or actions of nitric oxide (NO) have been implicated in the pathogenesis of glomerular hyperfiltration and hyperperfusion that occurs in early diabetes. However, the precise role of altered NO generation in the pathogenesis of diabetic nephropathy is unclear. The present study was aimed at investigating the role of nitric oxide in the pathogenesis of glomerular hyperfiltration and hyperperfusion in streptozotocin-induced diabetic rats. METHODS: To evaluate the role of NO in diabetic hyperfiltration, we measured plasma and urine concentrations of NO2-/NO3-, stable metabolic products of NO and protein expressions of three isoforms of nitric oxide synthase (NOS) in streptozotocin-induced diabetic rats. We also investigated renal hemodynamic changes, such as glomerular filtration rate (GFR) and renal plasma flow (RPF), in responses to acute and chronic administration of NO synthesis inhibitor, nitro-L-arginine methyl ester (L-NAME), in diabetic and control rats. RESULTS: Diabetic rats exhibited significantly elevated plasma and urinary NO2-/NO3- levels at 28 days after streptozotocin injection, and total excretion of NO2-/NO3- was approximately five-fold higher in diabetic rats than controls. Insulin and L-NAME treatment prevented the increases in plasma and urinary NO2-/NO3- concentrations in diabetic rats, respectively. The three isoforms of NOS (bNOS, iNOS, and ecNOS) were all increased in the renal cortex, whereas they remained unaltered in the renal medulla at day 28. GFR and RPF were significantly elevated in diabetic rats, and acute and chronic inhibition of NO synthesis by L-NAME attenuated the renal hemodynamic changes (increases in GFR and RPF) in diabetic rats, respectively. CONCLUSIONS: NO synthesis was increased due to enhanced NOS expression in diabetic rats, and chronic NO blockade attenuated renal hyperfiltration and hyperperfusion in diabetic rats. In addition, diabetic rats exhibited enhanced renal hemodynamic responses to acute NO inhibition and excreted increased urinary NO2-/NO3-. These results suggest that excessive NO production may contribute to renal hyperfiltration and hyperperfusion in early diabetes.
Animal ; Diabetes Mellitus, Experimental/physiopathology ; Diabetes Mellitus, Experimental/complications ; Diabetic Nephropathies/physiopathology ; Diabetic Nephropathies/etiology* ; Enzyme Inhibitors/pharmacology ; Male ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/biosynthesis* ; Nitric-Oxide Synthase/antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Renal Circulation/drug effects ; Support, Non-U.S. Gov't

The present study was aimed at investigating whether an altered role of nitric oxide (NO) is involved in chronic renal failure (CRF). Rats were subjected to 5/6 nephrectomy and kept for 6 weeks to induce CRF. On the experimental day, after measurement of arterial pressure under anesthesia, the arterial blood was collected, and thoracic aorta and kidney were rapidly taken. NO metabolites (NOx) were determined in the plasma, urine, aorta and kidney. The expression of NO synthase (NOS) isozymes was determined in the kidney and aorta by Western blot analysis. The expression of NOS mRNA in the glomeruli was also determined by RT-PCR. There were significant increases in arterial pressure and serum creatinine levels in CRF. Urine NOx levels were decreased in CRF, whereas plasma NOx levels were not altered. Aorta and kidney tissue NOx levels were also decreased in CRF. The expression of endothelial constitutive (ec) and inducible (i) isoforms of NOS proteins was decreased in the kidney and aorta in CRF. Accordingly, the expression of ecNOS and iNOS mRNA was decreased in the glomeruli in CRF. In conclusion, NO synthesis is decreased in the kidney and vasculature of CRF rats.
Animal ; Aorta, Thoracic/metabolism ; Comparative Study ; Enzyme Induction ; Isoenzymes/metabolism+ACo- ; Isoenzymes/genetics ; Kidney/metabolism ; Kidney Failure, Chronic/metabolism+ACo- ; Male ; Nephrectomy ; Nitrates/urine ; Nitrates/blood ; Nitric Oxide/deficiency+ACo- ; Nitric Oxide/biosynthesis ; Nitric-Oxide Synthase/metabolism+ACo- ; Nitric-Oxide Synthase/genetics ; Nitrites/urine ; Nitrites/blood ; Organ Specificity ; RNA, Messenger/biosynthesis ; Rats ; Rats, Sprague-Dawley