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Biomedical subjects

T Nakashima

Publications and source records attributed to T Nakashima.

At least 145 records · Page 8Linked to original sources

[A study on application of multiple jointed contact-type measuring apparatus for dental use].

The measurement of oral maxillofacial region, including dentition and teeth, is important information for diagnosis and assessment of treatment in clinical dentistry. There are two kinds of the measuring systems, i.e., contact-type system and non-contact-type system. The latter mainly has been investigated in dentistry, because of its simplicity and quickness for measurement. However, since the objects in dentistry have complex shapes with curved surfaces and many dead angles, accuracy of values obtained by this system is insufficient for clinical use. Even though divided measurement is employed to overcome the problems, the increase of measuring element results in deterioration of the accuracy. In the present study, the accuracy of a contact-type measuring apparatus with 5 pivoting joints was investigated. For the cavity model, the depth and the width were measured. For the standardized dental cast which consists of three spheres, the diameter of three spheres and the distance of each sphere were measured. The values obtained by this apparatus were compared with those obtained by the precise 3D-measurement apparatus. The differences were insignificant in the cavity model. Significant difference was found in the standardized dental cast. However, the difference was very small, and so it is negligible in clinical use. By using this apparatus, the form of undercut and teeth was reconstructed completely. The results suggested that the multiple jointed contact-type measuring apparatus could be applied to the measurement in clinical dentistry.

Dental Equipment↗

Glandular malignant peripheral nerve sheath tumor: an unusual case showing histologically malignant glands.

In this report, we describe a highly unusual case of glandular malignant peripheral nerve sheath tumor presenting as a neck mass in a previously healthy 29-year-old man. Grossly, the tumor was found to arise from a swollen peripheral nerve trunk. The tumor was largely composed of spindle cells that demonstrated marked nuclear pleomorphism and numerous abnormal mitotic figures. In addition, histologically malignant glandular structures lined by simple nonciliated columnar cells with goblet cells were found clustered in the center of the tumor. Examination of the swollen peripheral nerve trunk revealed the presence of a plexiform neurofibroma. The spindle cells were positive for S100. The glands were negative for S100 but positive for keratin, epithelial membrane antigen, and neuroendocrine markers (somatostatin, chromogranin, Leu-7, and calcitonin). This patient was subsequently diagnosed as having von Recklinghausen disease and died of tumor metastasis to the lungs 34 months after the presentation. To our knowledge, only 3 similar cases have been previously described in the literature.

Adult↗

[Coil embolization for incidental aneurysms in patients with chronic renal failure: midterm clinical results of two cases].

In spite of recent advances in perioperative management, the risk of neurosurgical intervention for patients with chronic renal failure is still considered too high. In this study, coil embolization for incidental aneurysms in such patients is demonstrated in reference to midterm results. A 42-year-old woman with a history of hemodialisis for 7 years presented with subcortical hemorrhage in her right frontal lobe. The magnetic resonance angiography (MRA) demonstrated a distal anterior cerebral artery aneurysm, but it was considered to be unrelated to the hemorrhage. Two and a half months after the hemorrhage the aneurysm was embolized with interlocking detachable coils. Thirty months after embolization, the angiogram revealed the coil compaction and the recanalization of the aneurysm neck. However, 54 months after embolization, the figure of the embolized aneurysm and neck remnant was the same as the previous findings. A 69-year-old woman with a history of hemodialisis for 5 years suddenly experienced left hemiparesis. Computed tomography revealed cerebral infarction in the right frontoparietal white matter. In addition, a left middle cerebral artery aneurysm was unexpectedly found on the MRA. Five months after the onset of the attack, the aneurysm was embolized with a Guglielmi detachable coli. An angiogram obtained 24 months after the embolization showed the aneurysm to be almost completely obliterated. In considering the therapeutic risks and benefits for incidental aneurysms of patients with chronic renal failure, intra-vascular surgery could be recommended as a less invasive treatment.

Adult↗

Air-bone gap and resonant frequency in large vestibular aqueduct syndrome.

BACKGROUND: Conductive hearing loss is occasionally recognized in large vestibular aqueduct (LVA) syndrome; however, the incidence rate and the cause are not known. OBJECTIVE: To compare air and bone conduction levels between patients with LVA syndrome and those with idiopathic sudden sensorineural hearing loss, and to investigate the cause of the air-bone gap. STUDY DESIGN: Retrospective study. SETTING: The patients were treated at a tertiary referral center. PATIENTS: Twenty-eight ears of 15 patients with LVA syndrome and 28 ears of patients with idiopathic sudden sensorineural hearing loss were examined. The latter patients were selected from a computerized database to match the former patients in air conduction levels. MAIN OUTCOME MEASURES: Pure-tone audiometry, multiple frequency tympanometry, acoustic reflex, otoacoustic emission, vestibular evoked myogenic response. RESULTS: The air-bone gap in patients with LVA syndrome was always larger than that in patients with idiopathic sudden sensorineural hearing loss with the same air conduction level. The resonant frequency in patients with LVA syndrome was rather low compared with that in normal control subjects, in contrast to the finding that resonant frequency was significantly high in patients with otosclerosis. CONCLUSIONS: An air-bone gap exists to some degree in almost all patients with LVA syndrome. The air-bone gap may not be associated with the movement restriction of the stapes as it is with otosclerosis.

Acoustic Impedance Tests↗

MR imaging of the enlarged endolymphatic duct and sac syndrome by use of a 3D fast asymmetric spin-echo sequence: volume and signal-intensity measurement of the endolymphatic duct and sac and area measurement of the cochlear modiolus.

BACKGROUND AND PURPOSE: In enlarged endolymphatic duct (EED) and sac (EES) syndrome, deformity of the EED and EES is congenital; however, hearing loss is acquired. To investigate the pathophysiology of progressive sensorineural hearing loss in EED and EES syndrome, we measured the volume of the EED and EES, the diameter of the EED and EES, the area of the cochlear modiolus, and the signal intensity of the EES and compared our findings against degree of hearing loss. METHODS: Thin-section MR images of 33 ears in 17 patients with EED and EES syndrome were studied. All studies were obtained on a 1.5-T MR unit using a quadrature surface phased-array coil. Heavily T2-weighted 3D fast asymmetric spin-echo images were obtained with a voxel size of 0.3 x 0.3 x 0.8 mm without zero-fill interpolation. Two radiologists traced the areas of the EED and EES manually, and the volume was calculated. The area of the cochlear modiolus, diameter of the EED and EES, and signal intensity of the EES were also measured by drawing regions of interest manually. The signal intensity ratio of EES/CSF was calculated. These measured values were compared against audiographic data, and the degree of linear correlation was determined. RESULTS: The volume of the EED and EES, the area of the modiolus, the diameter of the EED and EES, and the signal intensity of the EES did not show significant correlation with degree of hearing loss. CONCLUSION: These findings suggest that there is a microscopic area of damage or fragility in the inner ear not visible even with thin-section heavily T2-weighted MR imaging.

Adolescent↗

Large vestibular aqueduct syndrome treated by hyperbaric oxygen.

We report the case of a 14-year-old girl with a large vestibular aqueduct (LVA) in whom hyperbaric oxygen (HBO) therapy was effective for the treatment of sensorineural hearing loss. The patient was referred to Nagoya University Hospital for the treatment of hearing loss on 14 September, 1998, because her right hearing level had declined abruptly on 22 August, 1998, and had not changed for 3 weeks since then in spite of steroid and prostaglandin therapy. Her audiogram revealed bilateral profound deafness of more than 110 dB. She had had profound hearing loss on the left side since she was 9 years old. HBO therapy was performed on 22 occasions from 17 September until 19 October, 1998. During the HBO therapy, her right hearing ability returned almost to the level determined prior to the abrupt loss, 60 dB. We therefore recommend HBO therapy for the treatment of sensorineural hearing loss associated with large vestibular aqueduct syndrome if the hearing ability does not recover following conventional treatment.

Adolescent↗

Inhibition of caspase cascade by HTLV-I tax through induction of NF-kappaB nuclear translocation.

NF-kappaB is required for prevention of apoptosis. We examined the importance of human T-cell leukemia virus-I (HTLV-I) Tax protein to stimulate NF-kappaB nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study. Both Jurkat and Tax(-) JPX-9 cells had small amounts of basal nuclear NF-kappaB activity. The addition of NF-kappaB inhibitors suppressed NF-kappaB nuclear translocation of the cells, thus inducing apoptosis. Sequential activation of caspases from caspase-8 to caspase-3 was shown during this process. NF-kappaB nuclear translocation in JPX-9 cells was stimulated through Tax expression, and both the activation of caspases and apoptosis induced by NF-kappaB inhibitors were significantly suppressed in the Tax(+) JPX-9 cells. The expression of Bcl-2, Bax, and Bcl-x was not changed among Jurkat, Tax(-) JPX-9, and Tax(+) JPX-9 cells in the presence or absence of NF-kappaB inhibitors. X-chromosome-linked inhibitor of apoptosis (XIAP) protein expression in Tax(-) JPX-9 cells was significantly suppressed by NF-kappaB inhibitors, however, its expression in Tax(+) JPX-9 cells was maintained even by the addition of NF-kappaB inhibitors. Our results suggest that the activation of NF-kappaB via Tax protein in HTLV-I infected cells renders the cells resistant to apoptosis. The expression of anti-apoptotic gene products such as XIAP to suppress caspase cascade, results in an increase of cytokine production and cell proliferation; one of the proposed mechanisms that promotes autoimmune disorders such as Sjögren's syndrome and rheumatoid arthritis found in HTLV-I seropositive subjects.

Apoptosis↗

Identification and cDNA cloning of headpin, a novel differentially expressed serpin that maps to chromosome 18q.

Differential display was used to identify a novel serpin (headpin) underexpressed in squamous cell cancers of the oral cavity. Headpin cDNA encoding a complete open reading frame was cloned and sequenced. Headpin is expressed in normal oral mucosal tissue, skin, and cultured keratinocytes. Using Northern analysis and relative reverse-transcription polymerase chain reaction (relative RT-PCR), downregulation of headpin mRNA expression was demonstrated in oral cavity squamous carcinomas. Northern blot analysis identified a 3. 3-kb headpin mRNA transcript. Headpin is a 391-amino-acid protein with a theoretical molecular weight of 44 kDa. Hinge region homology at the reactive site loop suggests that headpin belongs to the inhibitory class of serine protease inhibitors. Headpin was mapped to 18q21.3/18q22. This region includes the ovalbumin serpins (ov-serpins) maspin, SCCA1, SCCA2, and PAI-2. Furthermore, 18q is recognized as a region for frequent loss of heterozygosity (LOH) in head and neck cancer and other malignancies.

Amino Acid Sequence↗

Ursodeoxycholic acid protects hepatocytes against oxidative injury via induction of antioxidants.

The therapeutic efficacy of ursodeoxycholic acid (UDCA) has been widely demonstrated in various liver diseases, suggesting that UDCA might protect hepatocytes against common mechanisms of liver damage. A candidate for such protection is oxidative injury induced by reactive oxygen species. This study was designed to assess the effects of UDCA on oxidative injury and antioxidative systems in cultured rat hepatocytes. The viability of the hepatocytes dose-dependently decreased after hydrogen peroxide or cadmium administration. Pretreatment with UDCA significantly prevented this decrease in viability. The amounts of glutathione (GSH) and protein thiol increased significantly, but the activities of antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and catalase were unchanged in UDCA-treated hepatocytes. The mRNA levels of gamma-glutamylcysteine synthetase and metallothionein (MT) were significantly higher in UDCA-treated hepatocytes than in controls. In conclusion, UDCA increased hepatocyte levels of GSH and thiol-containing proteins such as MT, thereby protecting hepatocytes against oxidative injury. Our results provide a new perspective on the hepatoprotective effect of UDCA.

Animals↗

Crystal structure of a ribonuclease from the seeds of bitter gourd (Momordica charantia) at 1.75 A resolution.

The ribonuclease MC1 (RNase MC1) from seeds of bitter gourd (Momordica charantia) consists of 190 amino acid residues with four disulfide bridges and belongs to the RNase T(2) family, including fungal RNases typified by RNase Rh from Rhizopus niveus and RNase T(2) from Aspergillus oryzae. The crystal structure of RNase MC1 has been determined at 1.75 A resolution with an R-factor of 19.7% using the single isomorphous replacement method. RNase MC1 structurally belongs to the (alpha+beta) class of proteins, having ten helices (six alpha-helices and four 3(10)-helices) and eight beta-strands. When the structures of RNase MC1 and RNase Rh are superposed, the close agreement between the alpha-carbon positions for the total structure is obvious: the root mean square deviations calculated only for structurally related 151 alpha-carbon atoms of RNase MC1 and RNase Rh molecules was 1.76 A. Furthermore, the conformation of the catalytic residues His-46, Glu-105, and His-109 in RNase Rh can be easily superposed with that of the possible catalytic residues His-34, Glu-84, and His-88 in RNase MC1. This observation strongly indicates that RNase MC1 from a plant origin catalyzes RNA degradation in a similar manner as fungal RNases.

Amino Acid Sequence↗

Modulation by endothelin-1 of lipopolysaccharide-induced cyclooxygenase 2 expression in mouse peritoneal macrophages.

We investigated the modulation by endothelin-1 of lipopolysaccharide-induced cyclooxygenase 2 expression and prostaglandin E2 production by mouse peritoneal macrophages. Our previous report showed that endothelin-1 at concentrations above 10(-11) M induced cyclooxygenase 2 expression through mainly endothelin ET(B) receptors and that an endothelin ET(B) receptor-mediated process was not involved in cyclooxygenase 2 activation in macrophages stimulated by lipopolysaccharide for 4 h. In the present study, when macrophages were stimulated by lipopolysaccharide for 12 h in the presence of endothelin-1 (10(-15) to 10(-8) M), cyclooxygenase 2 expression and prostaglandin E2 production were enhanced by 1.2- to 1.6-fold. The endothelin ET(B) receptor selective antagonist, BQ788 (N-cis-2,6-dimethylpiperidino-carbonyl-L-gamma-methyl-leucyl-D-L-m ethoxycarbonyl-tryptophanyl-norleucine), significantly inhibited this synergistic effect of endothelin-1. In addition, the cyclooxygenase 2-selective inhibitor, NS398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide), also suppressed this effect. Western blot analysis showed that the endothelin ET(B) receptor was up-regulated by lipopolysaccharide in a time- and concentration-dependent manner, and that this up-regulation was inhibited by NS398. From these results, we conclude that endothelin-1 promotes lipopolysaccharide-induced cyclooxygenase 2 activation in the delayed phase through endothelin ET(B) receptors up-regulated by lipopolysaccharide.

Animals↗

The three-dimensional structure of the RNA-binding domain of ribosomal protein L2; a protein at the peptidyl transferase center of the ribosome.

Ribosomal protein L2 is the largest protein component in the ribosome. It is located at or near the peptidyl transferase center and has been a prime candidate for the peptidyl transferase activity. It binds directly to 23S rRNA and plays a crucial role in its assembly. The three-dimensional structure of the RNA-binding domain of L2 from Bacillus stearothermophilus has been determined at 2.3 A resolution by X-ray crystallography using the selenomethionyl MAD method. The RNA-binding domain of L2 consists of two recurring motifs of approximately 70 residues each. The N-terminal domain (positions 60-130) is homologous to the OB-fold, and the C-terminal domain (positions 131-201) is homologous to the SH3-like barrel. Residues Arg86 and Arg155, which have been identified by mutation experiments to be involved in the 23S rRNA binding, are located at the gate of the interface region between the two domains. The molecular architecture suggests how this important protein has evolved from the ancient nucleic acid-binding proteins to create a 23S rRNA-binding domain in the very remote past.

Amino Acid Sequence↗

Cyclin D1 and p53 overexpression predicts multiple primary malignant neoplasms of the hypopharynx and esophagus.

BACKGROUND: Multiple primary upper aerodigestive tract carcinomas can occur in up to 15% of patients. We have shown previously that half of the patients with multiple upper aerodigestive tract squamous cell carcinomas are initially seen with synchronous tumors. Most metachronous squamous cell carcinomas become manifest within 3 years. OBJECTIVE: To examine the expression of 2 proteins-cyclin D1 and p53--in an attempt to predict the occurrence of multiple primary malignant neoplasms (MPs). MATERIALS AND METHODS: Monoclonal antibodies to cyclin D1 (DCS-6 [dilution, 1:50]. Novocastra Laboratories Ltd, Newcastle, England) and p53 (DO-7 [dilution, 1-100], Dako Corp, Carpinteria, Calif) proteins were used. Resection specimens from a total of 47 patients, 12 patients with MP and 35 patients with nonmultiple primary malignant neoplasms, were analyzed. Those in the nonmultiple primary malignant neoplasm group had longer than 3 years' follow-up to ascertain the absence of MP. RESULTS: Tumor overexpression of cyclin D1 was significantly associated with the development of MP (P<.01). Tumor overexpression of p53 was also frequent in patients with MP although statistical significance was not achieved. The combination of these 2 parameters was an even greater predictor of MP (P<.001). CONCLUSIONS: Overexpression of cyclin D1 and p53 proteins was highly correlated with the development of MP. Additional studies are necessary to confirm this finding. Immunohistochemical evaluation of primary squamous cell carcinomas for cyclin D1 and p53 overexpression may become an important fact of surgical pathologic reporting for primary upper aerodigestive tract squamous cell carcinomas.

Carcinoma, Squamous Cell↗

Regulation of synovial cell apoptosis by proteasome inhibitor.

OBJECTIVE: Recent studies have shown the importance of proteasome function in the regulation of apoptosis. This study examined whether inhibition of proteasome function mediates apoptosis of synovial cells, and whether cytokines modulate this process. METHODS: Type B synovial cells (fibroblast-like synovial cells) were cultured with tumor necrosis factor alpha (TNF alpha) or transforming growth factor beta1 (TGFbeta1), and further incubated in the presence of variable concentrations of Z-Leu-Leu-Leu-aldehyde (LLL-CHO), a proteasome inhibitor. During this process, apoptosis of synovial cells was determined by Hoechst 33258 dye staining and 51Cr release assay. The involvement of caspase cascade was examined using enzyme activity assay and blocking experiments by peptide inhibitors. The expression of pro-caspases, Bcl-2-related proteins, and X chromosome-linked inhibitor of apoptosis (XIAP) in synovial cells was examined by Western blot analysis. RESULTS: Apoptosis of cultured synovial cells was induced in a dose-dependent manner by LLL-CHO. Activation of caspase cascade through caspase-8 to caspase-3 was essential during this process. Pretreatment of synovial cells with TNF alpha significantly augmented both the activation of caspases and the proportion of apoptosis in synovial cells induced by LLL-CHO, whereas TGFbeta1 pretreatment markedly suppressed these phenomena. The ratio of the expression of Bcl-2 to Bax or Bcl-xL to Bax, and XIAP expression in synovial cells may not be directly associated with the susceptibility of synovial cells to apoptosis by LLL-CHO. CONCLUSION: Apoptosis of synovial cells was induced by inhibition of proteasome function through the activation of caspase cascade, and this process was clearly modulated by cytokines. These data provide new insight into the regulatory mechanisms controlling synovial cells in rheumatoid synovitis by proteasome inhibitors, and might be useful for the design of new therapeutic strategies in rheumatoid arthritis.

Apoptosis↗

A paucity of unusual trihydroxy bile acids in the urine of patients with severe liver diseases.

To clarify the relationship between the occurrence of unusual trihydroxy bile acids, namely hyocholic acid, ursocholic acid (UCA), and omega-muricholic acid (omega-MCA) in urine and liver disease severity, urinary bile acids were analyzed by gas-liquid chromatography in acute and late phases of acute hepatitis and before and after ursodeoxycholic acid (UDCA) loading in healthy adults and liver cirrhosis patients. In 11 patients with acute hepatitis, the occurrence rates and amounts of unusual trihydroxy bile acids were increased in the late (recovery) phase, as compared with those in the early phase. In 10 patients with severe acute hepatitis who had prothrombin times exceeding 16 seconds, these bile acids had completely disappeared from the urine in the early phase but reappeared in the late phase in those who had a good outcome, though never in a patient who died. After UDCA administration for a week, the amounts of unusual bile acids, especially UCA and omega-MCA, which are thought to be synthesized through 12 alpha- and 6 alpha-hydroxylations, respectively, from UDCA, were clearly increased in 10 healthy adults but only slightly changed in 10 patients with liver cirrhosis. In conclusion, hepatic hydroxylations of dihydroxy bile acids as a detoxification reaction were impaired in severe liver diseases, which may play a role in the intensification and perpetuation of hepatocellular injuries.

Acute Disease↗

Activation of caspase-8 in transforming growth factor-beta-induced apoptosis of human hepatoma cells.

Transforming growth factor-beta1 (TGF-beta1) has been shown to induce apoptosis in normal or transformed hepatocytes. To elucidate the biochemical pathways leading to apoptosis induced by TGF-beta1 in human hepatoma cells (HuH-7), we examined the expression of Bcl-2-related proteins and X-chromosome-linked inhibitor of apoptosis (XIAP), and activation of the caspase cascade following TGF-beta1 treatment. Bcl-xL expression began to decline at 12 hours after TGF-beta1 treatment and progressively decreased to very low levels in a time-dependent manner. Bax expression showed a little change throughout the experiment. On the other hand, activation of caspase-8 was clearly observed at 36 hours after TGF-beta1 treatment, followed by activation of caspase-9, and caspase-3 was activated at 48 hours after treatment at which time apoptosis of HuH-7 cells was observed. TGF-beta1 significantly decreased XIAP expression in HuH-7 cells. Addition of an inhibitor of caspase-8 or caspase-3 (IETD-FMK or DEVD-CHO) markedly inhibited TGF-beta1-induced apoptosis of HuH-7 cells. Fas/Fas ligand (FasL) interactions in HuH-7 cells were not involved in the apoptotic process. Furthermore, epidermal growth factor (EGF) also completely inhibited TGF-beta1-induced apoptosis of HuH-7 cells by inhibiting activation of the caspase cascade. Our results suggested that activation of caspase-3 initiated through caspase-8 activation is involved in the apoptotic process induced by TGF-beta1 in HuH-7 cells. Our results also showed that down-regulation of the expression of Bcl-xL and XIAP by TGF-beta1 may facilitate activation of caspase-3 in these cells.

Apoptosis↗