Synthesis of cage and ladder silsesquioxanes by the dehydration of silanols using dicyclohexylcarbodiimide (DCC) is described. The reaction of 1,3-dicyclohexyldisiloxane-1,1,3,3-tetraol with DCC gave octa(cyclohexylsilsesquioxane) in 13% yield. The bicyclic ladder siloxane 3 (Ph 8 Thex 2 Si 6 O 7 ) was prepared from 1,1,3,3tetraphenyldisiloxane-1,3-diol and 1,3-dithexyldisiloxane-1,1,3,3-tetraol (Thex or thexyl denotes 1,1,2-trimethylpropy) at 80°C. In this reaction, the propellane-type cage siloxane 2 (Ph 6 Thex 2 Si 5 O 6 ) was generated also. Upon reaction completion at 120°C, only 2 was obtained. The reaction from the same starting compounds with diisopropylcarbodiimide at 80°C resulted in another caged siloxane, Ph 4 Thex 4 Si 6 O 8 (5). The structures of 2, 3 and 5 were determined by X-ray crystallography.
Sirs, Compression of the left renal vein (LRV) between the aorta and the superior mesenteric artery (SMA), known as the nutcracker phenomenon (NCP), can cause gross or microscopic hematuria, flank pain, proteinuria, or a combination of these clinical features [1, 2, 3]. The phenomenon causes hypertension of the LRV, consequently causing LRV compression, left gonadal vein varices, and unilateral hematuria [2,4]. A recent report documented orthostatic proteinuria associated with the NCP [1, 5, 6, 7]. We describe two siblings with microscopic hematuria caused by NCP. These patients were a 3-year-old brother and a 5-year-old sister born to healthy non-consanguineous parents. Their family history manifested no renal diseases. Microscopic hematuria was first indicated in both patients by an annual screening urinalysis at their kindergarten. Their respective blood chemistries and urinary calcium/creatinine ratios were normal. Urine was normal except for sediment containing 5-20 red cells per high-power field. Repeated urine cultures showed no pathological organisms. Urinary red cell morphology revealed predominantly (>90%) isomorphic cells. Serum complement, IgA, IgG, and IgM concentrations, as well as antistreptolysin O titer, antinuclear antibody, antidouble-stranded DNA antibody, and rheumatoid factor were in the normal range. Ultrasonography of the kidneys showed marked dilatation of the LRV in the hilar portion and severe compression of the LRV between the aorta and the SMA, which was an indirect finding that is typical of NCP.
Sirs, A previously healthy 14-year-old boy presented with mild acute renal dysfunction with proteinuria and glucosuria. His past history and family history were unremarkable. The ophthalmologic examinations were normal. The patient was taking no medicines. Blood urea nitrogen of 18 mg/dl, creatinine of 1.3 mg/dl and creatinine clearance of 107.4 ml/min/1.73 m 2 were all measured. An autoantibody screen was negative. Urinary excretion of N-acetyl-beta-glucosaminidase (NAG) was 63.2 U/l (normal 0.3-11.5 U/l), and b2-microglobulin (b2-MG) was 37,079 g/l (normal 30-340 g/l). Serological tests for Epstein-Barr virus (EBV) showed the following: EBVviral capsid antigen (VCA) IgG 80x (negative <10x); VCA IgM <10x; early antigen-diffuse and restricted antibody (EA-DR) IgG <10x; EBV-nuclear antigen (EBNA) <10x. A cytomegalovirus (CMV)-specific IgM antibody showed a 1.27 index (negative <0.49 index) and a CMVspecific IgG avidity of 152 arbitrary units/ml (AU/ml; negative <14.9 AU/ml). Other serological results for hepatitis B, C, mycoplasmal pneumonia and syphilis were negative. Serial urine cultures showed no pathogens. A renal biopsy specimen showed marked lymphocytic tubulointerstitial nephritis (TIN) with tubular epithelial lesions and intratubular hyaline casts. The 30 glomeruli evaluated were completely normal, as were the blood vessels without granulomas and interstitial fibrosis. Immunofluorescent studies were negative. Immunohistochemical tests for CMV and EBV were negative. Mononuclear infiltration consisted mainly of CD3-positive lymphocytes with some CD8-positive T-cells and in small numbers of B-cells. Electron microscopy showed no evidence of viral inclusions. A CMV polymerase chain reaction (PCR) assay on peripheral blood was negative. Virus isolation from urine was not performed. The patient was given oral prednisolone (40 mg/day, 1 mg/kg/day, daily) with imidapril hydrochloride (5 mg/day) and showed a complete recovery. After rapid improvement of the clinical and laboratory signs of TIN, prednisone was tapered off over a period of 6 months without a flare-up of TIN.Acute TIN is a heterogeneous disorder that is caused by infectious agents, immunological disorders and idiopathic type. The patient had not taken nonsteroidal antiinflammatory drugs or any herbal or alternative medicines. The autoimmune screen and complement concentrations were normal, excluding autoimmune systemic diseases. Congenital and neonatal acute TIN is well known to be associated with CMV [1]. Recently, Kaminska et al. reported a case of CMV-associated TIN in a 15-year-old girl with positive CMV antigens in the kidney biopsy specimen [2]. Direct evidence of renal involvement with CMV infections is rarely seen. At the time of virus detection, CMV might have already disappeared from the targeted organ of the patient because older children and adults can rapidly eradicate CMV. Our case confirms CMV-related TIN only in part because the patient showed no symptoms of systemic CMV infection except for a fever, but the presence of IgM CMV antibo...
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