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141.
Al-Assir I Perez-Higueras A Florensa J Muñoz A Cuesta E 《AJNR. American journal of neuroradiology》2000,21(1):159-161
Percutaneous vertebroplasty is an effective treatment for many focal vertebral lesions. Methyl methacrylate is too viscous to be handled without difficulty in the conventional way because injection time is short. The operator is left with little time and must fumble with multiple syringes. We describe a special screw-system syringe that decreases the effort needed to inject the cement. In addition, it can standardize the injection pressures and control the injected volume because the threaded plunger affords greater control of injection pressure and volume delivered than does the conventional method. 相似文献
142.
García-Granero E Muñoz-Forner E Mínguez M Ballester C García-Botello S Lledó S 《Cirugía espa?ola》2005,78(Z3):24-27
Current treatment of chronic anal fissure continues to be based on conventional conservative measures in a high percentage of cases. What is known as chemical sphincterotomy aims to achieve a temporary decrease of anal pressures that allows fissures to heal. There are various alternatives such as nitroglycerine or diltiazem ointment and botulinum toxin injections. However, because of collateral effects and recurrences in the medium term, the definitive role of these treatments remains to be elucidated. Nevertheless, chemical sphincterotomy should be the first option in patients with a high risk of incontinence. "Open" or "closed" lateral internal sphincterotomy performed in the ambulatory setting with local anesthesia can currently be considered the ideal treatment of chronic anal fissure refractory to conservative measures so long as the patient is informed about the risk of minor incontinence. This procedure provides rapid and permanent recovery in more than 95% of patients. There is evidence demonstrating that the incontinence rate is related to the extent of the lateral internal sphincterotomy and consequently the extent of this procedure should be reduced to the length of the fissure. 相似文献
143.
Eduardo H. Garin Leila N. Diaz Wei Mu Clive Wasserfall Carlos Araya Mark Segal Richard J. Johnson 《Journal of the American Society of Nephrology : JASN》2009,20(2):260-266
CD80 is expressed on all antigen-presenting cells and is present on podocytes in a number of experimental models of nephrotic syndrome. We tested whether urinary soluble CD80 increased with idiopathic minimal-change disease (MCD). We collected urine and serum samples from patients with MCD in relapse and in remission, patients with nephrotic syndrome resulting from other glomerular diseases (FSGS, membranoproliferative glomerulonephritis, IgA nephropathy, and membranous nephropathy), patients with systemic lupus erythematosus, and normal control subjects. Urinary concentrations of soluble CD80 in patients with relapsed MCD were significantly higher compared with those observed in patients with MCD in remission, other glomerular diseases, and systemic lupus erythematosus with and without proteinuria and healthy control subjects. Urinary concentrations of soluble CTLA-4, which is a negative regulator of CD80, were not statistically different in patients with relapsed MCD compared with those in remission. The urinary soluble CD80/CTLA-4 ratio was >100-fold higher in patients with relapsed MCD compared with those in remission (P < 0.008). In contrast, serum concentrations of soluble CD80 and CTLA-4 did not distinguish patients with MCD in relapse and in remission. In conclusion, urinary soluble CD80 is elevated in idiopathic MCD, which could be relevant to both diagnosis and pathogenesis.Idiopathic minimal-change disease (MCD) is the most common nephrotic syndrome in children and adolescents.1 The disease is considered a disorder of T cell function.2,3 Although the mechanism of the proteinuria is unknown, a circulating cytokine has been postulated as the link between proteinuria and the T cell dysfunction.2–4Podocytes are specialized and highly differentiated epithelial cells that form a layer between the glomerular basement membrane and the urinary space. In a series of experiments, Reiser et al.5 found that these cells could acquire dendritic cell–like functions, in which they can be induced to express CD80, a transmembrane protein that provides a co-stimulatory signal for T cell activation. Mice administered LPS developed podocyte CD80 expression and proteinuria; when LPS was administered to the CD80−/− knockout mouse, no increase in urinary protein excretion was observed.5 The authors further showed that podocyte CD80 activation by LPS could occur in SCID mice that lack T cells.5 Furthermore, CD80 expression could be shown in both experimental models of nephrotic syndrome (e.g., aminonucleoside nephrosis) and human lupus nephritis.5 These findings led the authors to propose that podocyte CD80 expression might be involved in the pathogenesis of MCD.6Some podocyte antigens are known to be shed, where they can be found in the urine.7 This led us to hypothesize that soluble CD80 (sCD80) might be detected in the urine in patients with MCD. Furthermore, T regulatory cells are known to secrete soluble CTLA-4 (sCTLA-4), which can bind CD80 and block the co-stimulatory activation of T cells.8–10 If T cells are releasing a cytokine that can induce MCD, such as IL-13,11 then one might postulate that an inadequate release of sCTLA-4 might lead to continued activation of the T cells and possibly persistent CD80 expression by dendritic cells. We therefore measured urinary sCD80 and urinary sCTLA-4 levels in children with MCD and compared the findings with healthy children and children with other glomerular diseases.Clinical characteristics of the patients with MCD and control groups are shown in Patient Age (yr) Gender Diagnosis Urinary sCD80 (ng/g creatinine) Serum Albumin (g/dl) Up/Uc Ratio Treatment MCD in relapse 1 18 F 2114 3.9 1.1 Prednisone 60 mg/d 2 4 M 176 2.7 16.7 None 3 3 M 472 N/A 10.2 Prednisone 33 mg/d 4 2 F 156 3.2 3.8 None 5 1 M 473 N/A 13.1 Prednisone 18 mg every other day 6 13 M 503 3 5.2 Prednisone 5 mg every other day 7 8 F 936 2.2 7.9 Prednisone 15 mg/d 8 6 M 460 2 5.3 None 9 3 M 464 2.4 40.8 None 10 4 F 161 2.7 1.3 None 11 3 M 309 1.7 6.04 Prednisone 30 mg/d 12 16 F 216 N/A 14.5 Prednisone 10 mg every other day 13 5 M 2103 1.3 17.6 Prednisone 30 mg/d 14 2 F 849 2.7 4.2 Prednisone 15 mg twice a day 15 2 M 919 1.6 10.2 Prednisone 30 mg/d mean ± SEM 6 ± 1 687 ± 163 2.5 ± 0.2 10.5 ± 2.6 MCD in remission 3 3 M 110 N/A Neg Prednisone 30 mg/d 4 2 F 43 3.2 <0.61 None 5 3 M 12 N/A 0.32 Prednisone 30 mg/d, cyclosporine 30 mg twice a day 6 13 M 51 N/A 0.08 Prednisone 60 mg/d 7 8 F 13 3.4 <0.33 Prednisone 42 mg/d 9 3 M 7 N/A 0.2 Prednisone 30 mg/d 10 4 F 14 N/A Neg Prednisone 9 mg every other day 11 3 M 69 N/A 0.17 Prednisone 30 mg/d 16 2 M 11 3.3 <0.47 Prednisone 30 mg/d, cyclosporine 30 mg twice a day 17 3 F 94 4 0.16 Prednisone 7 mg every other day, MMF 200 mg twice a day, Prograf 1.5 mg twice a day 18 8 F 51 N/A <0.23 None 19 10 M 23 3.6 <0.48 Prednisone 60 mg/d, cyclosporine 25 mg morning and 100 mg afternoon mean ± SEM 5 ± 1 41 ± 10 3.5 ± 0.1 0.25 ± 0.07 Other glomerular diseases 20 12 M FSGS 18 1.9 14.9 None 21 17 F FSGS Undetected 3.4 2.05 None 22 13 M FSGS Undetected 3.9 1.64 None 23 13 M FSGS 22 4.1 1.12 None 24 13 F MPGN 78 3.3 8.55 Prednisone 60 mg every other day 24 13 F MPGN 48 3.2 4.8 Prednisone 60 mg every other day 25 10 F Membranous nephropathy 154 11.5 Prednisone 40 mg every other day, Cytoxan 50 mg/d 26 16 F Membranous nephropathy 42 2.3 2.27 Prednisone 20 mg every other day, cyclosporine 125 mg twice a day 27 11 F Membranous nephropathy 158 3.3 6.8 None 28 22 F IgA nephropathy 14 4 1.2 None 29 6 F IgA nephropathy 79 0.57 None mean ± SEM 13 ± 1 55 ± 17 3.3 ± 0.3 5.03 ± 1.45 Control subjects 30 15 M 137 <0.06 N/A 31 18 F 5 0.19 N/A 32 16 M 2 0.06 N/A 33 4 mo M 28 Neg N/A 34 20 F 15 Neg N/A 35 3 F 8 Neg N/A 36 1 F 152 Neg N/A 37 5 F 13 Neg N/A 38 9 mo F 164 Neg N/A mean ± SEM 8 ± 2 58 ± 23 0.03 ± 0.02 Patients with SLE 39 40 F Neg prot 162 Prednisone 5 mg/d, Cellcept 1.5 g/d 40 59 F 0.09 70 N/A 41 10 F 0.16 255 Prednisone 20 mg/d, Cellcept 750 mg twice a day 42 25 F 0.16 124 Imuran 150 mg/d 43 25 F 0.17 111 None 44 37 F 0.18 122 Prednisone 10 mg/d 45 46 F 0.22 37 Cellcept 1 g twice a day 46 50 M 0.24 10 Prednisone 60 mg/d 47 43 F 0.29 7 N/A 48 44 F 0.31 65 Prednisone 15 mg/d 49 32 F 0.35 444 None 50 48 F <0.4 0 Prednisone 2.5 mg every other day, methotrexate 17.5 mg/wk 51 28 F 0.47 38 Prednisone 30 mg/d, Imuran 150 mg/d 52 9 M 0.53 159 Methylprednisolone 1 g intravenously 53 41 F 0.88 577 N/A 54 29 F 0.96 37 Cellcept 1 g twice a day 55 20 F 1.25 55 Cellcept 1.5 g twice a day 56 44 F 1.3 35 N/A 57 36 M 3.32 80 Cellcept 1.5 g twice a day 58 17 F 8.35 122 Prednisone 10 mg/d, Cellcept 750 mg twice a day 59 17 F 8.35 24 Prednisone 30 mg/d, Cellcept 1.5 g twice a day mean ± SEM 33 ± 3 1.34 ± 0.53 127 ± 31