Acquired Fanconi syndrome due to long-term adefovir administration in a patient with IgG-kappa monoclonal gammopathy and kappa Bence-Jones protein.

A 77-year-old man was admitted to our hospital for a right femoral neck fracture. He had been prescribed lamivudine for chronic hepatitis B infection for 11 years, and adefovir was added 5 years ago. After hospitalization, a right femoral head prosthesis was performed successfully, but an unknown hypokalemia was revealed. Hypophosphatemia, hypouricemia, glucosuria, and panaminoaciduria were also revealed, and multiple microfractures were detected by bone scintigraphy. We diagnosed him as 'osteomalacia associated with Fanconi syndrome,' which was likely due to the adefovir. Moreover, a monoclonal IgG-kappa and a kappa Bence-Jones protein were detected in his serum and urine, respectively. We switched from adefovir plus lamivudine to entecavir and started calcitriol. His excessive urinary ß2-microglobulin excretion and glucosuria had decreased dramatically at 10 weeks after the modification of drugs; those of the phosphate, uric acid and total protein, however, continued. Renal biopsy specimens obtained at 10 weeks after discontinuation of adefovir revealed focal tubular atrophic changes with/without inflammatory cells, which were predominantly observed next to glomeruli. Kappa-dominant staining was not observed in either glomeruli or tubules with immunostaining by the enzyme-labeled antibody method. Electron microscopy revealed neither crystalline structures in the cytoplasm of proximal tubules nor electron-dense deposits. Because of the remarkable proportional reduction of other urinary protein fractions, urinary M-peak appeared 26 weeks after discontinuation of adefovir, but the net amounts of the fraction decreased gradually.

Inducing alpha-helices in short oligopeptides through binding by an artificial hydrophobic cavity.

Short peptides were induced into alpha-helix conformations in water through enclathration to an artificial hydrophobic cavity. Peptides with two aromatic residues showed high affinity for the host, and these intermolecular aromatic-aromatic interactions specifically drove the helical folding of short peptides.

Microvascular response in the periosteum following mucoperiosteal flap surgery in dogs: 3-dimensional observation of an angiogenic process.

BACKGROUND: An increase in blood flow from the periosteum after mucoperiosteal flap surgery is essential for healing and angiogenesis and repair may work in close cooperation to facilitate this process. To investigate the role of the periosteal vascular plexus in the healing process, we used 3-dimensional (3-D) and ultrastructural monitoring of the angiogenic process after elevation of the mucoperiosteal flap. METHODS: Mucoperiosteal flap surgery was performed on nine adult beagle dogs. The periosteal vascular plexus was observed 3, 5, and 7 days after surgery in histological specimens in which blood vessels were injected with India ink under a light microscope, in ultrathin sections under a transmission electron microscope, and in acryl plastic vascular cast specimens under a scanning electron microscope. RESULTS: On day 3 after surgery, new blood vessels, formed through sprouting, bridging, and intussusception, were observed in ultrathin sections and vascular casts. In addition, blood island-like structures consisting of clustered immature endothelial cells were noted in the repaired tissue. On days 5 to 7 after surgery, 3-D observation of vascular casts clarified that these new blood vessels had a sinus-like morphology in the interstitium of the periosteal vascular plexus. These new sinusoidal vessels exhibited a stereoscopic structure with increased continuity as the blood vessels matured and ultrastructurally the vascular endothelium was thinned. CONCLUSIONS: After mucoperiosteal flap elevation, the periosteal vasculature exhibited potent blood vessel-forming activity through various angiogenic mechanisms and through repair activity. Our results provide a 3-dimensional clarification that the periosteal vascular plexus has an important role in the healing process after flap surgery.

Relationship between position of probe tip and periodontal tissues after periodontal surgery in dogs.

The aim of this study was to investigate postsurgical periodontal probe penetration by using clinical information and histometric data. Thirty-eight three-walled defects were created in four dogs, then maintained for 3 months. Subsequently, 26 defects were subjected to periodontal surgery (surgical group), while 12 defects served as controls. The dogs were sacrificed at 4, 8, 12, and 16 weeks. Immediately before sacrifice, endodontic silver points were placed in the gingival crevices as substitutes for periodontal probes and fixed on the teeth. Following block sections, histologic and histomorphometric evaluations were undertaken: location of the probe tip in relation to the apical termination of the junctional epithelium, length of new junctional epithelium in relation to the apical junctional epithelium, and mean length of connective tissue adhesion in relation to the apical junctional epithelium. Probe tips were located -1.37 +/- 1.73 mm and -0.20 +/- 0.15 mm apical to the apical junctional epithelium for the surgical and control groups, respectively, at 4 weeks, while the probe tip was located 0.58 +/- 0.31 mm and 0.40 +/- 0.20 mm coronal to the apical junctional epithelium, respectively, at 16 weeks. Length of new junctional epithelium in relation to apical junctional epithelium was significantly less for the surgical than the control group at 4 weeks (0.73 +/- 0.60 mm vs 1.19 +/- 0.02 mm) and 8 weeks (1.77 +/- 0.52 mm vs 2.15 +/- 0.00 mm). There were no significant differences between the groups in regard to connective tissue relationship to the apical junctional epithelium. Periodontal probing is not recommended for at least 2 months after surgical procedures; before this stage, probing forces may damage the soft tissue-tooth interrelationship.