Durability of tungsten carbide burs for the fabrication of titanium crowns using dental CAD/CAM

The purpose of this study was to evaluate the durability of tungsten carbide burs for the fabrication of titanium crowns using two dental CAD/CAM systems (DECSY, Digital Process, Japan and Cadim, Advance, Japan). A tungsten carbide bur in each system was examined and used without fracture to fabricate 51 titanium crowns. For both systems tiny chips were found on the bur blade at the 11th machining. These chips gradually enlarged as the number of machining times increased. At the first machining no significant difference in the average surface roughness was found on the crown between the two systems (1.6 microm for DECSY and 1.2 microm for Cadim). The cutting grooves became dull and the average surface roughness increased as the number of machining times increased. It is concluded that the tungsten carbide burs for both systems can be used to fabricate up to 51 titanium crowns.     

BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions

BACKGROUND: High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. METHODS: We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. RESULTS: BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. CONCLUSION: In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy.     

Urothelial cancer producing granulocyte colony-stimulating factor: possible induction of splenomegaly

Approximately 33% of patients with renal cell carcinoma will present with metastases. Patients have a reported 35% 5-year survival rate in instances in which nephrectomy and surgical resection of a solitary metastasis have been performed. Laparoscopic partial nephrectomy has become an increasingly viable option in the treatment of some renal cancers. We report a case in which a patient had a solitary lung nodule in the workup for a renal mass. This patient underwent combined thoracoscopic and laparoscopic resection of both the lung nodule and the renal mass in the same setting.     

Incremental benefits of FDG positron emission tomography over CT alone for the preoperative staging of ovarian cancer

OBJECTIVE: The purpose of this study was to determine whether the addition of positron emission tomography (PET) with the radiotracer FDG to cross-sectional imaging, such as CT, increases accuracy in the detection of tumor spread. SUBJECTS AND METHODS. Fifteen patients who were thought to have ovarian cancer on the basis of the results of physical examination, sonography findings, and level of serum cancer antigen 125 were enrolled over an 11-month period. After screening, patients underwent two imaging examinations-abdominopelvic CT and whole-body FDG PET- within 2 weeks before surgery. Also before surgery, staging accuracy was assessed separately using CT with or without FDG PET (which was based on modifications of the International Federation of Gynecology and Obstetrics [FIGO] criteria). The results of the histology and surgery findings were used to assess the accuracy of the scanning findings. RESULTS: Staging revealed stage III disease in seven patients (IIIC, n = 6; IIIB, n = 1), stage II in three (IIC, n = 2; IIB, n = 1), and stage I in five (IC, n = 3; IA, n = 2), according to the FIGO criteria. Although CT staging correlated with postoperative staging in eight (53%) of 15 patients, consensus evaluation of CT with FDG PET staging improved correlation with postoperative staging in 13 (87%) of 15 patients. CONCLUSION: The addition of FDG PET to CT increases accuracy in staging of ovarian cancer.     

Differences in the contribution of HLA-DR and -DQ haplotypes to susceptibility to adult- and childhood-onset type 1 diabetes in Japanese patients

To clarify heterogeneity in Japanese adult-onset type 1 diabetes, we analyzed the HLA-DR and -DQ haplotypes, depending on the clinical phenotype, and compared them with those in childhood-onset type 1 diabetes (CO). The patients in a previously reported Ehime Study were divided into subgroups by the mode of onset of diabetes: 68 acute-onset type 1 diabetic patients (AO) and 28 slowly progressive type 1 diabetic patients (SO). HLA haplotypes were compared with those of 80 CO patients and 190 control subjects. Two major susceptible HLA haplotypes in the Japanese, DRB1*0405-DQB1*0401 (DR4) and DRB1*0901-DQB1*0303 (DR9), were significantly increased in the AO and CO groups, but only DR9 was increased in the SO group. AO subjects had a higher frequency of DR9 than CO subjects. Accordingly, the DR9:DR4 frequency increased with increasing age of onset. Another susceptible haplotype, DRB1*0802-DQB1*0302 (DR8), was involved only in the CO group. Analysis of haplotype combinations revealed that DR4 and DR9 had significant dosage effects on the AO and CO groups (P < 0.0001), but only DR9 had such an effect in the SO group (P < 0.03). These results suggest differences in the contribution of HLA class II haplotypes to susceptibility of type 1 diabetes depending on the clinical phenotype and also indicate that HLA class II haplotypes may be associated with the onset age of type 1 diabetes.     

The etiologic role of intrauterine volvulus and intussusception in jejunoileal atresia

Purpose

Although intussusception has been reported as quite a rare cause of jejunoileal atresia (JIA), pediatric surgeons have noted the frequent presence of intussusception as well as volvulus at surgery. The aim of this study was to investigate the contribution of intrauterine intussusception and volvulus to the development of JIA.

Methods

In 48 newborns (24 boys and 24 girls) treated for JIA at our hospital between 1978 and 2004, the operative and pathologic findings were reviewed.

Results

Intussusception was responsible for gap and cord type atresia in 12 cases (25%). The cord showed an atrophic intestinal lumen in 2 cases. Volvulus was observed in 13 cases. Volvulus and intussusception were simultaneously noted in 1 case. This suggested that intussusception was the cause of the atresia, whereas volvulus was a secondary event. Neither intussusception nor volvulus was observed in high jejunal, apple peel, or multiple atresia.

Conclusions

Intrauterine volvulus and intussusception were commonly observed in single mid- and low JIA. Thus, intrauterine intussusception may be a common cause of gap and cord type JIA. Volvulus may not only cause JIA but also result from anatomic changes after the development of JIA in some cases.     

Morphologic change and astrocyte response to unilateral spinal cord compression in rabbits

In myelopathy, unilateral compression of the spinal cord in cases of disc herniation would be expected to produce Brown-Séquard syndrome. However, a transverse lesion syndrome occurs in most clinical cases. In order to reveal the mechanism by which unilateral compression induces transverse damage to the spinal cord, damage of the gray and white matter in each half of the spinal cord were evaluated quantitatively to determine the density of GFAP-positive astrocytes. The cervical spinal cord in rabbits was unilaterally compressed with a small screw. The area of each half of the damaged cord and the density of GFAP-positive astrocytes of the compressed and contralateral halves were investigated one week after the surgery. No apparent paralysis was observed during the period of observation. As the compression increased, the area of the compressed half of the spinal cord decreased significantly compared to the contralateral half. The densities of GFAP-positive astrocytes in the gray matter and the anterior funiculus increased significantly in the compressed half. There were no significant differences in the densities at the lateral and dorsal funiculi between the compressed and contralateral halves. The tissue damage in the gray matter of the compressed half was markedly higher. No significant difference between the two halves in damage was seen in the lateral funiculus, where in the lateral pyramidal and the dorsal spinocerebellar tracts are found. These findings provide evidence of the mechanistic basis for the spinal cord damage that leads to transverse lesion syndrome in unilateral compression myelopathy.     

Comparison of ropivacaine with bupivacaine and lidocaine for ilioinguinal block after ambulatory inguinal hernia repair in children

BACKGROUND: We have compared ropivacaine with bupivacaine and lidocaine for ilioinguinal block in thirty children undergoing ambulatory inguinal hernia repair. METHODS: Patients were assigned randomly to receive 0.5 ml.kg(-1) of 0.2% ropivacaine (Group R, n = 10), 0.25% bupivacaine (Group B, n = 10) or 1% lidocaine (Group L, n = 10). The patients' parents, who were not informed of the type of local anaesthetic employed, evaluated the postoperative pain at 2 h and 6 h after operation using the Wong-Baker FACES Pain Rating Scale. RESULTS: There was a significant difference in the face scale score between Group R and Group L, and Group B and Group L. There was no difference in the face scale score between Group R and Group B. There were no complications or clinical evidence of local anaesthetic toxicity. CONCLUSIONS: We have confirmed that bupivacaine and ropivacaine are more effective than lidocaine in the prevention of postoperative pain after children's inguinal hernia repair. We suggest that ropivacaine 0.2% is an alternative to bupivacaine 0.25% for ilioinguinal block in ambulatory paediatric surgery.     

Ebselen inhibits p38 mitogen-activated protein kinase-mediated endothelial cell death by hydrogen peroxide

Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis.