Two-level posterior lumbar interbody fusion for degenerative disc disease: improved clinical outcome with restoration of lumbar lordosis

BACKGROUND CONTEXT: Although posterior lumbar interbody fusion (PLIF) for degenerative lumbar diseases is routine, there are few reports on double-level PLIF. PURPOSE: To evaluate the clinical outcomes of double-level PLIF. STUDY DESIGN/SETTING: A retrospective study of operated cases in Gifu, Japan. PATIENT SAMPLE: Nineteen patients (8 men and 11 women, 59.5+/-10.2 years) who underwent double-level PLIF between 1996 and 2001. OUTCOME MEASURES: Operation time, blood loss, complications, the Japanese Orthopaedic Association (JOA) score for back pain and lumbar sagittal alignment were evaluated. METHODS: Patients were examined retrospectively at follow-ups of 3.6+/-1.7 years. Primary diseases were spondylolisthesis, spinal canal stenosis, degenerative scoliosis and herniated intervertebral disc. Fusion areas were L3 to L5 in 15 cases and L4 to S1 in 4 cases. RESULTS: The mean JOA score increased from an initial score of 12.9+/-3.5 to 21.3+/-4.9 at the final follow-up. There was a positive correlation (R=0.718, p<.001) between the increase in lordotic angle and the increase in the JOA score. Several parameters suggested that the surgical invasiveness was not minimal. CONCLUSION: Double-level PLIF provided satisfactory results and preserved lumbar spine lordosis.     

Pharmacokinetics of fluorinated 2-nitroimidazole hypoxic cell radiosensitizers in murine peripheral nervous tissue.

We have previously reported that KU-2285, a 2-nitroimidazole with a fluorinated N1-substituent (-CH2-CF2CONH(CH2)nOH, n = 2), was a promising hypoxic cell radiosensitizer. In this study the pharmacokinetics of KU-2285 and its related compounds (n = 3 and n = 4) were compared with those of etanidazole (a 2-nitroimidazole with an N1-substituent of -CH2CONH(CH2)nOH, n = 2) and its related compounds (n = 3 and n = 4) to assess the effects of incorporation of a CF2 group. The lipophilicity of the fluorinated compounds was higher than that of etanidazole, as measured by the octanol/water partition coefficient. As the number of CH2 groups increased, the lipophilicity of the compounds in both the KU-2285 and etanidazole series increased. The brain tissue levels of the fluorinated compounds were as low as those of the etanidazole derivatives, while the biological half-lives of the fluorinated compounds in peripheral nervous tissues were shorter than those of related non-fluorinated compounds.     

Intravenous immunoglobulin therapy for Guillain-Barré syndrome in Japan: changes in treatment after its inclusion in health insurance coverage]

In December 2000, health insurance in Japan was instituted for the use of intravenous immunoglobulin (IVIg) therapy for the acute phase of Guillain-Barré syndrome (GBS) that required aid to walk or worse. A nation-wide questionnaire survey was made to investigate the changes in treatment. In September 2002, a letter of inquiry was sent to experienced physicians in 620 teaching hospitals associated with the Societas Neurologica Japonica and 417 associated with the Societas Paediatrica Japonica. Totally, 356 neurologists (57%) and 223 pediatricians (53%) responded. After the introduction of IVIg health insurance coverage, more than 90% thought that GBS patients should be hospitalized and given treatment. The frequency of hospitals with an intensive care unit, however, was 70%. Before IVIg therapy's inclusion in health insurance coverage, many neurologists selected plasmapheresis (88%) rather than IVIg (4%) therapy, whereas pediatricians preferred IVIg (49%) to plasmapheresis (12%). After its inclusion, 75% of neurologists selected IVIg rather than plasmapheresis (21%), whereas pediatricians selected IVIg (86%) over plasmapheresis (5%). In March 2003, new payment system based on Diagnosis Procedure Combination was introduced into 82 large hospitals, and leads to difficulties to select IVIg in the hospitals. The payment system should be revised.     

A rare case of cerebral aspergillus aneurysm at the site of temporary clip application

Anterior communicating artery aneurysm was shown in a 48-year-old man who had suffered from subarachnoid hemorrhage (SAH) by cerebral angiography. Right pterional approach was performed on the 40th day after SAH. Premature ruptured occurred during aneurysmal manipulation and temporary clip (Scoville clip) was placed at the middle of the right A1 segment for fifteen minutes. the anterior communicating artery aneurysm was successfully clipped and postoperative course was uneventful. But, four days after the operation, the patient fell into coma following generalized tonic convulsion. Lumbar puncture showed fresh SAH. Consciousness recovered gradually to a lethargic state. A newly formed berry aneurysm was revealed on the righ A1 segment at the site of the temporary clip application by cerebral angiography performed on the seventh day after aneurysmal surgery. Second attack occurred on the 12th postoperative day and the patient died on the 16th day after the operation. Postmortem findings disclosed massive subarachnoid and intraventricular hemorrhage from the ruptured aneurysm at the right A1 segment. Microscopic examination of the aneurysm and the right A1 segment. microscopic examination of the aneurysm and the right A1 segment showed the extensive destruction of the artery and massive proliferation of aspergillus in the arterial wall which was prominent of its outer layer. The mechanism of the formation of the new aneurysm in this case was considered as follows: the arterial wall was primarily damaged by the temporary clip and was weakened rapidly by the invasion of aspergillus, probably producing thrombosis of the vast vasorum, hemorrhage, and necrosis in it.     

Study on the extent of peritumoral edema in glioma: its correlation with the proliferative potential and tumor-infiltrating mononuclear cells]

The correlation between the extent of peritumoral edema and the proliferative potential or the infiltration of mononuclear cells was studied in 17 gliomas. The peritumoral edema was evaluated on contrast enhanced CT scan as the ratio of the low density area around the tumor to the enhanced high density area. The proliferative potential and the infiltration of mononuclear cells into the tumor were investigated immunohistochemically using monoclonal antibody (MAb) against DNA polymerase alpha and anti-Leu MAb's respectively. There was a significant correlation between the extent of the peritumoral edema and the percentage of DNA polymerase alpha positive cells. The degree of the infiltration of mononuclear cells into the tumor tissue also correlated with the extent of peritumoral edema. In gliomas with high proliferative potential and/or severe infiltration of mononuclear cells, the peritumoral edema may be aggravated by disruption of the blood-brain-barrier and increased vascular permeability.     

Cyclic adenosine monophosphate production and contractile response induced by beta-adrenoceptor subtypes in rabbit urinary bladder smooth muscle

The spontaneous contractile force of muscle strips isolated from male rabbit urinary bladder dome [detrusor) and base (trigonal muscle) was dose dependently inhibited by isoproterenol, a non-specific beta-adrenoceptor agonist. The relaxant response to 10(-6) M isoproterenol in the detrusor muscle was completely blocked by butoxamine (10(-4) M), a selective beta-2-antagonist, and by propranolol (10(-6) M), a non-specific beta-antagonist, but not by metoprolol (10(-6) to 10(-4) M), a selective beta-1-antagonist. Relaxation of trigonal muscle induced by 10(-6) M isoproterenol was inhibited 30% by metoprolol (10(-5) M), 70% by butoxamine (10(-4)M), and 100% by propranolol (10(-6) M). Terbutaline, a selective beta-2-adrenoceptor agonist, also caused dose dependently a relaxant response in detrusor and trigonal muscle. The maximum relaxant responses to isoproterenol and terbutaline were significantly greater in detrusor than in trigonal muscle. Dobutamine, a relatively specific beta-1-adrenoceptor agonist, caused a small but significant relaxant response in trigonal, but no change in detrusor muscle. In trigonal muscle the relaxant response to dobutamine was less than that to terbutaline. Cyclic adenosine monophosphate accumulation in detrusor did not significantly increase after administration of dobutamine, but significantly increased after administration of terbutaline. On the other hand, not only terbutaline, but also dobutamine, markedly increased cyclic adenosine monophosphate accumulation in trigonal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary artery reoperation utilizing "free" gastroepiploic artery

A 57-year-old female underwent coronary artery bypass reoperation successfully by utilizing the free gastroepiploic artery (GEA) graft in combination with the in situ left internal mammary artery (IMA) graft. The left IMA was anastomosed to the left anterior descending artery and the "free" GEA was anastomosed to the left IMA proximally and to the first diagonal branch distally. The patient recovered well with a disappearance of angina. Postoperative angiogram at 6 weeks showed good patency of both grafts and improvement of left ventricular contraction was obtained. Thus, GEA can be utilized not only as an "in situ" graft, but also as a "free" graft, effectively.     

Cell sheet engineering: recreating tissues without biodegradable scaffolds

While tissue engineering has long been thought to possess enormous potential, conventional applications using biodegradable scaffolds have limited the field's progress, demonstrating a need for new methods. We have previously developed cell sheet engineering using temperature-responsive culture dishes in order to avoid traditional tissue engineering approaches, and their related shortcomings. Using temperature-responsive dishes, cultured cells can be harvested as intact sheets by simple temperature changes, thereby avoiding the use of proteolytic enzymes. Cell sheet engineering therefore allows for tissue regeneration by either direct transplantation of cell sheets to host tissues or the creation of three-dimensional structures via the layering of individual cell sheets. By avoiding the use of any additional materials such as carrier substrates or scaffolds, the complications associated with traditional tissue engineering approaches such as host inflammatory responses to implanted polymer materials, can be avoided. Cell sheet engineering thus presents several significant advantages and can overcome many of the problems that have previously restricted tissue engineering with biodegradable scaffolds.     

A hamster temperature-sensitive G1 mutant, tsBN250 has a single point mutation in histidyl-tRNA synthetase that inhibits an accumulation of cyclin D1

Background: We have previously isolated a series of temperature-sensitive mutants for cell-proliferation from the BHK21 cell line, derived from the golden hamster. These mutants proliferate at 33.5 °C, the permissive temperature, but not at 39.5 °C the restrictive temperature. Using DNA-mediated gene transfer, human genes complementing these ts mutants were cloned.
Results: At 39.5 °C the tsBN250 cell line, a temperature-sensitive mutant of the BHK21 cell line, had a defect in the G1 phase, but not in the S phase. The human gene complementing tsBN250 cells was found to encode histidyl-tRNA synthetase. Indeed, the tsBN250 cell line had a single base change—guanine to adenine at the second position of the 362nd codon of hamster histidyl-tRNA-synthetase, converting arginine to histidine. Following release from serum starvation, cyclin E, but not cyclin D1, was accumulated, while, at 39.5 °C, the mRNA of cyclin D1 was normally expressed in tsBN250 cells. A similar inhibition of cyclin D1 accumulation was observed in another ts mutant, tsBN269, which has a single point mutation in lysyl-tRNA synthetase. Overexpression of cyclin D1 enabled tsBN250 cells to enter the S phase.
Conclusion: tsBN250 cells have a single point mutation in histidyl tRNA synthetase that causes a loss of histidyl-tRNA synthetase activity which in turn reduces the content of cyclin D1, but not of cyclin E, thereby resulting in G1 arrest.