A modified technique of renal artery anastomosis in rat kidney transplantation.

AIMS: To reduce warm ischemic time and avoid irreversible damage to the graft in rat kidney transplantation. METHODS: After left nephrectomy, recipients were transplanted with syngeneic kidney grafts using microsurgical techniques. In control rats (n = 20), the renal artery anastomoses were performed with 8-9 interrupted sutures by the conventional technique. In experimental animals (n = 20), a modified anastomosis was performed using fewer (5-6) sutures and fibrin glue devoid of thrombin. RESULTS: The number of sutures in the control group was 8.09 + or - 0.35 while that in the experimental group was 5.65 + or - 0.48 (p < 0.01). The warm ischemic time reduced from 29.7 + or - 1.1 min in the control group to 23.9 + or - 0.9 min in the experimental group (p < 0.01). These anastomoses maintained adequate patency rates and mechanical strength. Up to 21 days after operation, the graft survival rates in the experimental and control groups were 90 and 85%, respectively. CONCLUSIONS: Our modified technique for renal artery anastomosis significantly reduced the warm ischemic time in rat kidney transplantation. This technique would be a safe and reliable method for rat renal artery anastomosis as well as for other microarterial anastomoses, particularly for novice surgeons.

Presynaptic morphological changes associated with long-term synaptic facilitation are triggered by actin polymerization at preexisting varicositis.

Morphological changes are thought to contribute to the expression of long-term synaptic plasticity, a cellular basis for learning and memory. The mechanisms mediating the initiation and maintenance of the morphological changes are poorly understood. We repeatedly imaged the axonal arbors of mechanosensory neurons of Aplysia as they formed new synaptic varicosities and axonal branches after applications of serotonin that cause long-term synaptic facilitation. New varicosities formed exclusively from preexisting varicosities, by splitting or branch outgrowth. These changes were prevented by cytochalasin D, which blocks actin polymerization and the turnover of actin filaments. The suppression of the morphological changes by cytochalasin D did not impair their expression when cytochalasin D was removed 24 hr after exposure to serotonin. These results imply that serotonin induces persistent effects at preexisting presynaptic varicosities, which enhance actin polymerization, and that this is essential for presynaptic morphological changes of long-term facilitation.

A 19F-NMR study of the membrane-binding region of D-lactate dehydrogenase of Escherichia coli.

D-Lactate dehydrogenase (D-LDH) is a membrane-associated respiratory enzyme of Escherichia coli. The protein is composed of 571 amino acid residues with a flavin adenine dinucleotide (FAD) cofactor, has a molecular weight of approximately 65,000, and requires lipids or detergents for full activity. We used NMR spectroscopy to investigate the structure of D-LDH and its interaction with phospholipids. We incorporated 5-fluorotryptophan (5F-Trp) into the native enzyme, which contains five tryptophan residues, and into mutant enzymes, where a sixth tryptophan is substituted into a specific site by oligonucleotide-directed mutagenesis, and studied the 5F-Trp-labeled enzymes using 19F-NMR spectroscopy. In this way, information was obtained about the local environment at each native and substituted tryptophan site. Using a nitroxide spin-labeled fatty acid, which broadens the resonance from any residue within 15 A, we have established that the membrane-binding area of the protein includes the region between Tyr 228 and Phe 369, but is not continuous within this region. This conclusion is strengthened by the results of 19F-NMR spectroscopy of wild-type enzyme labeled with fluorotyrosine or fluorophenylalanine in the presence and absence of a nitroxide spin-labeled fatty acid. These experiments indicate that 9-10 Phe and 3-4 Tyr residues are located near the lipid phase.

Kyphoplasty for the treatment of very severe osteoporotic vertebral compression fracture.

OBJECTIVE: A retrospective evaluation of the clinical outcome and technical feasibility of kyphoplasty for the treatment of very severe osteoporotic vertebral compression fracture (vsOVCF). METHODS: Patients with vsOVCF were treated with kyphoplasty and followed-up for 1 year. Vertebral body height variation, kyphotic angle, back pain (visual analogue scale [VAS]) and Oswestry disability index (ODI) were evaluated preoperatively, postoperatively, 1 month, 3 months and 1 year after treatment. RESULTS: In total, 35 patients (49 vertebrae) were treated with kyphoplasty. There were no cases of spinal or extraspinal injury, infection, bleeding, pulmonary embolism, epidural cement leakage, stroke or cardiac arrest as a result of treatment. There were significant postoperative improvements in all outcome measures (vertebral body height variation, kyphotic angle, VAS and ODI); these improvements were maintained during the follow-up period. CONCLUSION: Kyphoplasty is an effective and minimally invasive procedure for the treatment of vsOVCF.