We experienced a rare case of a 54-year-old male with a burst fracture of the axis body (C-2). The mechanism of this lesion was thought to be application of a vertical downward force and bending force to the dense. On arrival, he had severe pain on his neck and neurological deficit on his left upper extremity. Plain radiography and CT scan showed a burst fracture of the axis body classified as type 2 according to Benzel's classification. He was treated with direct traction for the first six weeks and halo-vest fixation for the next four weeks. We kept his neck in an extension position opposing the mechanism of injury. Three months later, reduction and bone union were obtained. Eleven months after injury, he had no neck pain and neurological symptoms, and the motion range of the cervical spine was not restricted. The fragments were united by conservative therapy.Our case suggested that the mechanism of this fracture was axial downward force with flexion position.

64歳，男性．約2.5m高より転落し，当科救急外来搬送された．意識清明で全身に多数の打撲傷，口腔内出血を認めた．腰痛と左下肢の疼痛を訴え，徐々に左下肢の皮膚温低下，運動，知覚麻痺，皮膚色調変化が進行した．左大腿動脈以下の動脈拍動が触知不能であった．下顎骨骨折と第4腰椎椎体の骨折を認めたが，脊柱管内への骨片の突出はなかった．腹部造影CTで腰椎骨折部に隣接する左総腸骨動脈の外傷性解離による閉塞を認めた．左下肢阻血に対する循環動態改善のため，緊急で左総腸骨動脈結紮術と大腿動脈―大腿動脈バイパス術を施行した．術後，左下肢の循環動態は改善し，左下肢痛，運動，知覚障害とも速やかに回復した．術後1年4ヵ月の現在は機能障害なく現職に復帰している．受傷機転は腰椎の過伸展強制により動脈が牽引されたものと推察された．腰椎骨折に合併した総腸骨動脈解離は稀有であるが，重篤な外傷であるため，迅速な対応が必要である．

The purpose of this study was to examine the correlation between preoperative complications and hospital expenses in femoral intertrochanteric fractures. We studies 34 patients who were hospitalized and operatad on in our hospital. The hospital expenses of patients who had preoparative complications were higher. The difference between those with and without the complications was almost 120,000 yen. But treatment expenses for the complications were less than expected. We found that hospital expenses increased in proportion to the duration of hospitalization, indicationg that increase in hospital expenses is not due to the cost of the treatment for complications but rather for the extended duration of hospitalization. We concluded that shortening the duration of hospitalization is an adequate means of reducing hospital expenses.

OBJECTIVETGFbeta is a potent stimulator of cell growth in cultured rat articular chondrocytes (CRAC). The stimulatory effect is mediated through the immediate induction of c-fos gene by activating ERK of MAPK. The present study was undertaken to investigate the upstream regulators involved in TGFbeta-induced ERK activation in CRAC and to compare the results with the events in HepG2 cells.RESULTSIn vitro kinase and trans-reporting assays showed that TGFbeta preferentially activated ERK and JNK pathways in CRAC and HepG2, respectively. ERK activation in CRAC was selectively inhibited by PD98059, a MEK inhibitor. Overexpression of wild or active forms of MEKK1, the upstream activator of ERK and JNK, decreased the TGFbeta-induced 3TP-luciferase activity in CRAC. In contrast, in HepG2 dominant negative form of MEKK1 or SEK1 ligand-dependent reporter activity was diminished. Transfection of TAK1, another MAPKKK, also positively and negatively regulated 3TP transcriptional activity of HepG2 and CRAC, respectively. Activation of PKA by 8-bromo-cyclic AMP or forskolin, and inhibition of PKC by calphostin C, resulted in a significant decrease in 3TP activity as well as in vitro ERK kinase activity in CRAC.CONCLUSIONSThe results indicate that TGFbeta transduces a predominant signal pathway through MEK-ERK-Elk1, independent of MEKK1 or TAK1 pathway in CRAC. However, in HepG2, activation of MEKK1 and TAK1 is essential for TGFbeta-induced signal transmission. The results also demonstrated that in CRAC, MEK-ERK pathway activated by TGFbeta is negatively regulated by PKA cascade but transactivated by PKC.

Intraarticular injection of dexamethasone (DEX) accelerates cartilage degradation due to the suppression of chondrocyte proliferation and extracellular matrix formation. The present study first demonstrated the interaction between DEX and TGF beta, a potent growth factor for cultured rat articular chondrocytes (CRAC), and then investigated the molecular mechanism by which DEX counteracts TGF beta-induced chondrocyte proliferation and differentiation through the regulation of AP-1 activity. DEX reduced serum-deprived and TGF beta-stimulated cell growth and [(3)H]-thymidine incorporation of CRAC. DEX also inhibited the expression of (alpha)1 type II collagen with concomitant suppression of the promoter activity. Transfection studies using a reporter vector with AP-1 responsive elements showed that DEX reduced TGF beta-activated but not basal luciferase activities. Activation of 3TP-luc, another AP-1 responsive element containing reporter was also blocked by DEX. GAL4-Elk1 studies revealed that DEX suppressed TGF beta-induced ERK activation which led to c-fos gene expression followed by increase in AP-1 complex formation, whereas the Smad pathway was not involved in DEX-dependent negative regulation of AP-1 in a reporter assay that requires FAST1-Smad2 for the activation. DEX also eliminated TGF beta-induced c-fos mRNA expression and ERK activation in Northern analysis and in vitro kinase assay, respectively. Further, DNA synthesis and transactivation of type II collagen by TGF beta were inhibited by PD98059, an inhibitor of MEK. Our results indicate that DEX suppressed TGF beta-induced chondrocyte proliferation and type II collagen expression, probably through selective inhibition of ERK integrated AP-1 activation.

OBJECTIVE To investigate the involvement of Tie-1 and Tie-2, receptor tyrosine kinases required for angiogenesis, in synovial proliferation and angiogenesis of rheumatoid arthritis (RA). METHODS Synovial tissues from 10 patients with RA and three control subjects were analysed by double immunohistochemistry and reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS Expression of Tie-1 and Tie-2 was seen in all synovia, but predominantly in papillary projected portions. In synovial lining cells, Tie-2 was expressed mainly in the basal layer and frequently colocalised with vimentin and proliferating cell nuclear antigen (PCNA), whereas Tie-1 was also expressed in the superficial layer. In stromal cells, Tie-2 immunoreactivity was restricted to vimentin positive fibroblast—but not macrophage derived cells, whereas Tie-1 expression was not dependent on the phenotype. Tie receptors were also highly expressed in the endothelium and surrounding pericytes of capillaries scattered over the papillary proliferated synovium without notable difference in the expression of the two receptors. Furthermore, Tie positive vessels often overexpressed PCNA. In normal synovia, expression of Tie receptors was restricted to the capillary endothelium. RT-PCR confirmed the expression of Tie-1 and Tie-2 in RA synovial tissues and also in the cultured synoviocytes. CONCLUSION The results suggest the possible involvement of overexpressed Tie-1 and Tie-2 in synovial lining and stromal cells in the pathophysiology of RA synovitis, probably through distinct mechanisms. Furthermore, expression of Tie receptors in actively growing vasculature may reflect the direct involvement of these receptors in angiogenesis and subsequent vascularisation.

Transforming growth factor-beta1 (TGF-beta1) stimulates articular chondrocyte cell proliferation and extracellular matrix formation. We reported previously that immediate and transient expression of c-fos mRNA through protein kinase C activation is required for the mitogenic effect of TGF-beta1 on cultured rat articular chondrocytes (CRAC). In gel kinase assays using myelin basic protein (MBP) showed that total cell lysates from cells treated with TGF-beta1 caused rapid phosphorylation of MBP, which suggests the involvement of mitogen-activated protein kinase (MAPK) activation. To identify specific MAPK pathways activated by TGF-beta1, we performed in vitro kinase assays using specific substrates. TGF-beta1 induced a rapid activation of extracellular signal regulated kinase (ERK) with a peak at 5 min, which decreased to basal levels within 240 min after TGF-beta1 stimulation. In contrast, the c-jun N-terminal kinase activity increased only about 2.5-fold after 240 min of stimulation and p38 MAPK activity did not change significantly. ERK activation by TGF-beta1 was also confirmed by in vivo phosphorylation assays of Elk1. However, a specific MEK1 inhibitor, PD98059, significantly decreased TGF-beta1 induced Elk1 phosphorylation in a dose-dependent manner. Furthermore, PD98059 reduced the TGF-beta1-induced cell growth by 40%. These results indicate that TGF-beta1 specifically activates MEK1 and subsequent ERK pathways in CRAC, and that the activation of this MAPK pathway plays a role in the mitogenic response to TGF-beta1.

Smad proteins are known to transduce signalling of TGF-beta receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and 5' RACE. The predicted amino acid sequences of rat Smad2 and Smad4 are highly conserved among rat, human and mouse. We also mapped these Smads to chromosome 18q.12.3. Unlike endothelial cells, TGF-beta1 stimulates articular chondrocyte proliferation as well as extracellular matrix production, and acts as a repairing agent against cartilage destruction. Since both Smad2 and Smad4 are essential factors for TGF-beta signalling, we examined their expression and regulation in cultured articular chondrocytes. Northern blot analysis showed that TGF-beta1 significantly increased the mRNA level of Smad2 but not of Smad4 in a dose- and time-dependent manner, suggesting that the augmentation of TGF-beta1 action is caused by increasing the expression of the downstream signalling molecule.

Miller-Galante typeII total knee replacement (TKR) has been performed in our department since March 1991. We report our evaluation of TKR performed for rheumatoid arthritis particularly looking at bilateral TKR carried out at the same time (B-TKR).B-TKR is compared to unilateral TKR and gradual bilateral TKR in this report.We found that B-TKR has the advantages of decreasing the patient's physical, mental and economic burden. However, it increases the surgical and anesthetic burden.

The function of disordered lumbosacral nerve roots in cases of transitional vertebrae was studied from the viewpoint of neurological findings.There were 25 cases who had a single neve root disorder. The level of the transitional vertebrae (T. V.) was calculated from the cephalic side, which were classified into 2 groups; (1) S Type (lumbar number 4+T. V.), (2) L Type (lumbar number 5+T. V.). The function of the transitional nerve roots were S type in 10 cases and L type in 15 cases In addition there were a lot of mixed nerve root disordered cases which were composed of both L5 and S1 factors.Moreover in the L type, the function of the transitional nerve roots was influenced by the shape of the transverse process and the level of the iliac crest.From these results, it was suggested that the function of the nerve roots was influenced by the shape of the bone.

We studied the MRI findings of 2 desmoid tumors in the supraclavicular fossa. One case was a 30 year-old woman and another was a 22 year-old man. The Tumor of Case 1 consisted almost totally of collagen fibers and showed a low signal intensity in both T1 and T2-weighted images. In comparison, the tumor of case 2 was found to be more hypercellular, similar to a benign fibrous histiocytoma. The intensity of both T1-weighted and T2-weighted images of Case 2 was higher than those of Case 1. MRI was available to evaluate the extent of the tumor, but no specific signal intensity was noted.

A rare case of pathological dislocation of the hip in von Recklinghausen's disease is reported.A 13-year-old boy suddenly developed pain and dislocation of his right hip with no obuious cause. He visited our department 8 months after onset of symptoms for right hip pain and a limp. He had many typical café au lait spots on his skin and bilateral anterior leg angulation. Neurofibroma were detected by skin biopsy. Radiographs demonstrated right femoral head deirtion to the supra-lateral side, t femur was atrophic femur and both acetabula were hypoplastic. Joint effusion of the right hip was seen on MR I and arthrtgraphy. CT showed hypoplasia of both acetabul a and an irregular margin of the right acetabulum with bone multiplication. We proposed that this pathological dislocation was caused by decreasing restriction and congruity of the hip joint. The former is due to relaxation of the joint capsle, and the latter is due to the irregular acetabular surface caused by invasion of neurofibroma.