Cystadenocarcinoma in the maxillary sinus with high-grade carcinoma component.
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Cystadenocarcinoma↗
Biomedical subjects
K Mishima
Publications and source records attributed to K Mishima.
Evaluation of respiratory status and mandibular movement after total temporomandibular joint replacement in patients with rheumatoid arthritis.
We performed total TMJ replacement to improve respiratory status and correct occlusion in six patients with destruction of the temporomandibular joint (TMJ) caused by rheumatoid arthritis. Morphological changes were evaluated on lateral cephalograms before and after surgery. Respiratory function and mandibular movement were assessed with the use of an apnea-monitor and an LED mandibular tracking device, respectively. After surgery, symptoms such as snoring and daytime sleepiness improved, and solid food could be masticated. Postoperative cephalograms showed that both the posterior airway space and ramal height were significantly improved by surgery. Postoperative records of mandibular movement indicated stability of the occlusion and improvement of mandibular movement, as compared with the preoperative records. Mean oxygen saturation significantly improved 1 month after surgery, whereas apnea and apnea-hypopnea indices did not change significantly.
Aged↗
Small foci of high-grade carcinoma cells in adenoid cystic carcinoma represent an incipient phase of dedifferentiation.
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Carcinoma, Adenoid Cystic↗
Juxtaoral organ of Chievitz presenting clinically as a tumour.
An extremely rare hamartomatous lesion of the juxtaoral organ of Chievitz (JOOC) in a 63 year old man is reported. The tumour appeared as a large mass in the infratemporal fossa with associated mandibular bone resorption; histologically, it was well encapsulated and composed of numerous tangled masses of benign squamous epithelial nests and mature fibrofatty tissue. There were no histological features suggestive of neoplastic transformation. A literature survey confirmed that this is the first adult case of JOOC presenting clinically as an extraoral tumour.
Biomarkers↗
Salivary cystatins influence ingestion of capsaicin-containing diets in the rat.
Dietary capsaicin consumed by rats over several days induces cystatin-like substances in submandibular saliva. Yet the physiological role of these salivary proteins has not been thoroughly investigated. Salivary cystatins in the rat submandibular glands are known to be induced by chronic treatment with the sympathetic beta-agonist, isoproterenol. In the present study, the possible roles of the salivary proteins on food intake were examined by comparing consumption of a capsaicin-adulterated (0.05%) diet in rats with and without isoproterenol pretreatment (0.1 and 5.0 mg/kg, 5 days). Electrophoretic analysis performed prior to feeding trials revealed that the group pretreated with 5 mg/kg isoproterenol had large amounts of cystatin in the saliva compared with the group pretreated with 0.1 mg/kg isoproterenol and control group. The group treated with 5 mg/kg isoproterenol showed greater consumption of the capsaicin-adulterated diet than the other groups until the 3rd day of trials. Bilateral removal of the submandibular and sublingual glands neutralized the effects of isoproterenol. Induction of salivary cystatins by isoproterenol treatment was not mimicked by systemic and intragastric administration of capsaicin. These results suggest that cystatins are included in the salivary proteins induced by capsaicin and that they contribute to enhanced ingestion of the capsaicin diet. Induction of salivary cystatins may be triggered by irritation of the oral mucosa by capsaicin.
Analysis of Variance↗
Application of dynamic laser scattering to the quality control of injectable drugs: polymer formation in ampicillin solution.
OBJECTIVE: To assess the usefulness of dynamic laser scattering for monitoring the stability of ampicillin after reconstitution from commercially available vials with respect to the polymer formation and potency. METHODS: Polymer formation and the remaining potency of the reconstituted ampicillin solution were estimated using dynamic laser scattering and high-performance liquid chromatography. RESULTS: The laser light-scattering submicron particle analyser was sufficiently sensitive for detecting both monomer and polymer aggregates with the average diameter of 1.1 +/- 0.2 and 7.3 +/- 1.7 nm, respectively, in the ampicillin solution. Polymer formation was dependent on both the storage temperature and the storage period, but it was detected, even when no precipitates were visible and when loss of potency was less than 10% of the initial value following storage at 4 or -15 degrees C. CONCLUSION: Submicron particle analysis using scanning electron microscopy, when used in combination with high-performance liquid chromatography, provides a useful method for studying polymer formation in antibiotic solutions and for the quality control of antibiotic injections during storage.
Ampicillin↗
The protein tyrosine phosphatase TCPTP suppresses the tumorigenicity of glioblastoma cells expressing a mutant epidermal growth factor receptor.
Glioblastoma multiforme (GBM) is the most aggressive type of glioma and GBMs frequently contain amplifications or mutations of the EGFR gene. The most common mutation results in a truncated receptor tyrosine kinase known as Delta EGFR that signals constitutively and promotes GBM growth. Here, we report that the 45-kDa variant of the protein tyrosine phosphatase TCPTP (TC45) can recognize Delta EGFR as a cellular substrate. TC45 dephosphorylated Delta EGFR in U87MG glioblastoma cells and inhibited mitogen-activated protein kinase ERK2 and phosphatidylinositol 3-kinase signaling. In contrast, the substrate-trapping TC45-D182A mutant, which is capable of forming stable complexes with TC45 substrates, suppressed the activation of ERK2 but not phosphatidylinositol 3-kinase. TC45 inhibited the proliferation and anchorage-independent growth of Delta EGFR cells but TC45-D182A only inhibited cellular proliferation. Notably, neither TC45 nor TC45-D182A inhibited the proliferation of U87MG cells that did not express Delta EGFR. Delta EGFR activity was necessary for the activation of ERK2, and pharmacological inhibition of ERK2 inhibited the proliferation of Delta EGFR-expressing U87MG cells. Expression of either TC45 or TC45-D182A also suppressed the growth of Delta EGFR-expressing U87MG cells in vivo and prolonged the survival of mice implanted intracerebrally with these tumor cells. These results indicate that TC45 can inhibit the Delta EGFR-mediated activation of ERK2 and suppress the tumorigenicity of Delta EGFR-expressing glioblastoma cells in vivo.
Animals↗
Total sleep deprivation induces an acute and transient increase in NK cell activity in healthy young volunteers.
STUDY OBJECTIVES: To investigate the effects of one night's total sleep deprivation (TSD) on NK cell activity, with rigorous control of circadian phase of sampling points as well as physical exercise level in association with sleep deprivation. DESIGN: The mean sleep onset time of each subject before starting the study was defined as his 0000 h. This study was composed of a Sleep-Sleep session (sleep times, 00:00 h - 08:00 h and 24:00 h - 32:00 h) and a Sleep-Wake session (sleep time, 00:00 h - 08:00 h) with TSD (24:00 h - 32:00 h) placed in a cross-over design with 2-week interval between each session. In each session, the subjects were rested in the supine position under dim light from - 06:00 h to 36:00 h (for 42 hours). SETTING: University-based sleep and chronobiology laboratory PARTICIPANTS: 10 healthy adult men (mean age, 20.9 y; age range, 19-23 y) INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: NK cell activity was measured every 4 hours from 12:00 h. NK cell activity during TSD (at 28:00 h) has been revealed to significantly increase (p=0.01) compared with the corresponding value in the Sleep-Sleep session. This effect was weaker at their usual waking time 32:00 h (p=0.07), and disappeared until 36:00 h (4 hours after awakening). The circadian rhythm phases (dim light melatonin onset time) were coincident between the 2 sessions. CONCLUSIONS: The present findings suggest that one night TSD induces an acute and transient increase in NK cell activity that is not influenced by the effects of circadian rhythm or the amount of physical exercise undertaken during TSD.
Adult↗
Environmentally benign formation of polymeric microspheres by rapid expansion of supercritical carbon dioxide solution with a nonsolvent.
A novel method is reported for forming polymer microparticles, which reduce atmospheric emissions of environmentally harmful volatile organic compounds such as toluene and xylene used as paint solvent in paint industry. The polymer microparticles have formed through rapid expansion from supercritical solution with a nonsolvent (RESS-N). Solubilization of poly(styrene)-b-(poly(methyl methacrylate)-co-poly (glycidyl methacrylate)) copolymer(PS-b-(PMMA-co-PGMA), MW = 5000, PS/PMMA/PGMA = 2/5/3), poly(ethylene glycol) (PEG, M. W = 4000), bisphenol A type epoxy resin (EP, MW = 3000), poly(methyl methacrylate) (PMMA; MW = 15000, 75000, 120000), and poly(oxyalkylene) alkylphenyl ether (MW = 4000) in carbon dioxide (CO2) was achieved with the use of small alcohols as cosolvents. The solubility of the PS-b-(PMMA-co-PGMA) is extremely low in either CO2 or ethanol but becomes 20 wt % in a mixture of the two. Because ethanol is a nonsolvent for the polymer, it can be used as a cosolvent in rapid expansion from supercritical solution to produce 1-3 microm particles that do not agglomerate. Obtained polymer particles by RESS-N were applied as powder coatings. The resulting coatings have a smooth and coherent film. The particle size distribution of microspheres was controlled by changing the polymer concentration, preexpansion pressure, temperature, and injection distance. The feed compositions were more effective than the other factors in controlling the particle size. The polymeric microparticles formed by RESS-N method can be utilized to make the thin coating film without anytoxic organic solvents and/or surfactants.
Absorption↗
Restoration of endogenous wild-type p53 activity in a glioblastoma cell line with intrinsic temperature-sensitive p53 induces growth arrest but not apoptosis.
p53 protein is a transcription factor involved in multiple tumor-suppressor activities including cell cycle control and apoptosis. TP53 gene is frequently mutated in glioblastoma, suggesting the importance of inactivation of this gene product in gliomagenesis. Restoration of p53 function in glioblastoma cell lines deficient for p53 has shown that p53 induces growth arrest or apoptosis depending on the cell line and vector used to transduce wild-type TP53 alleles. Considering that astrocytes grow and express p53, it is not clear whether these results reflect physiologic responses or the result of p53 overexpression in combination with cellular responses to viral vector infection. Here, we reassessed this issue using a glioblastoma cell line (LN382) that expresses an endogenous temperature-sensitive mutant p53. This cell line expresses TP53 alleles (100% as determined by a p53 transcriptional assay in yeast) mutated at codon 197 GTG (Val) > CTG (Leu). We found that the p53 protein in these cells acted as an inactive mutant at 37 degrees C and as a functional wild-type p53 below 34 degrees C as demonstrated by several lines of evidence, including (i) restoration of transactivating ability in yeast, (ii) induction of p53-modulated genes such as CDKN1(p21) and transforming growth factor-alpha, (iii) disappearance of accumulated p53 protein in the nucleus and (iv) decrease in steady state p53 protein levels. This temperature switch allowed p53 levels, which were close to physiological levels to dramatically reduce LN382 cell proliferation by inducing a G(1)/S cell cycle block, but not to induce apoptosis. The lack of apoptosis was considered to be a result of the low level p53 expression, because increasing wild-type p53 levels by adenoviral-mediated gene transfer caused apoptosis in these cells. The LN382 cell line will be extremely useful for investigations into the roles of p53 in cellular responses to a variety of stimuli or damages.
Apoptosis↗
Effects of endothelin on adrenomedullin secretion and expression of adrenomedullin receptors in rat cardiomyocytes.
Both endothelin (ET) and adrenomedullin (AM), produced by cardiac myocytes, are thought to be locally-acting hormones in the heart. Recently, calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMPs) have been shown to function together to serve as AM receptors stimulating cAMP production. In the present study, we examined the effects of ET on AM secretion, intracellular cAMP response to AM, and gene expressions of CRLR and RAMPs in cultured cardiac myocytes. Synthetic ET-1 dose-dependently increased AM secretion from the cardiomyocytes. AM increased the intracellular cAMP level in a dose-dependent manner and the cAMP accumulation by AM was significantly amplified by 24 h preincubation with ET-1. 10 nmol/L ET-1 significantly increased the CRLR mRNA level without any effect on RAMP1 mRNA. 1 micromol/L ET-1 significantly reduced the RAMP2 mRNA level, but ET-1 dose-dependently increased the RAMP3 mRNA level in the cardiac myocytes. These findings suggest that ET-1 not only stimulates AM secretion, but also modulates intracellular cAMP responses to AM probably by altering the expressions of CRLR and RAMPs in rat cardiomyocytes.
Adrenomedullin↗
Ameliorative effect of vasopressin-(4-9) through vasopressin V(1A) receptor on scopolamine-induced impairments of rat spatial memory in the eight-arm radial maze.
In order to clarify the mechanism by which pGlu-Asn-Cys(Cys)-Pro-Arg-Gly-NH(2) (vasopressin-(4-9)), a major metabolite C-terminal fragment of [Arg(8)]-vasopressin (vasopressin-(1-9)), improves learning and memory, we used several different drugs such as an acetylcholine receptor antagonist, a Ca(2+)/calmodulin-dependent protein kinase II inhibitor, vasopressin receptor antagonists and L-type Ca(2+) channel blocker to disrupt spatial memory in rats. Moreover, we examined the effect of vasopressin-(4-9) on acetylcholine release in the ventral hippocampus using microdialysis. Vasopressin-(4-9) (10 fg/brain, i.c.v.) improved the impairment of spatial memory in the eight-arm radial maze induced by scopolamine, pirenzepine and Ca(2+)/calmodulin -dependent protein kinase II inhibitor. Pirenzepine, a vasopressin V(1A) receptor antagonist, and L-type Ca(2+) channel blocker, but not a vasopressin V(2) receptor antagonist, suppressed the effects of vasopressin-(4-9) on scopolamine-induced impairment of spatial memory. Moreover, vasopressin-(4-9) did not affect acetylcholine release in the ventral hippocampus of intact rats or of scopolamine-treated rats as assessed by microdialysis. These results suggest that vasopressin-(4-9) activates vasopressin V(1A) receptors on the postsynaptic membrane of cholinergic neurons, and induces a transient influx of intracellular Ca(2+) through L-type Ca(2+) channels to interact with muscarinic M(1) receptors. The activation of these processes by vasopressin-(4-9) is critically involved in the positive effect of vasopressin-(4-9) on scopolamine-induced impairment of spatial memory.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Growth suppression of intracranial xenografted glioblastomas overexpressing mutant epidermal growth factor receptors by systemic administration of monoclonal antibody (mAb) 806, a novel monoclonal antibody directed to the receptor.
A mutant epidermal growth factor receptor (variously called DeltaEGFR, de2-7 EGFR, or EGFRvIII) containing a deletion of 267 amino acids of the extracellular domain is frequently highly expressed in human malignant gliomas and has been reported for cancers of the lung, breast, and prostate. We tested the efficacy of a novel monoclonal anti-DeltaEGFR antibody, mAb 806, on the growth of intracranial xenografted gliomas in nude mice. Systemic treatment with mAb 806 significantly reduced the volume of tumors and increased the survival of mice bearing xenografts of U87 MG.DeltaEGFR, LN-Z308.DeltaEGFR, or A1207.DeltaEGFR gliomas, each of which expresses high levels of DeltaEGFR. In contrast, mAb 806 treatment was ineffective with mice bearing the parental U87 MG tumors, which expressed low levels of endogenous wild-type EGFR, or U87 MG.DK tumors, which expressed high levels of kinase-deficient DeltaEGFR. A slight increase of survival of mice xenografted with a wild-type EGFR-overexpressing U87 MG glioma (U87 MG.wtEGFR) was effected by mAb 806 concordant with its weak cross-reactivity with such cells. Treatment of U87 MG.DeltaEGFR tumors in mice with mAb 806 caused decreases in both tumor growth and angiogenesis, as well as increased apoptosis. Mechanistically, in vivo mAb 806 treatment resulted in reduced phosphorylation of the constitutively active DeltaEGFR and caused down-regulated expression of the apoptotic protector, Bcl-XL. These data provide preclinical evidence that mAb 806 treatment may be a useful biotherapeutic agent for those aggressive gliomas that express DeltaEGFR.
Animals↗
Microdialysates of amines and metabolites from core nucleus accumbens of freely moving rats are altered by dizocilpine.
In vivo microdialysis combined with high performance liquid chromatography (HPLC) with electrochemical detection, was used to study the effect of MK-801 (0.1 mg/kg i.p.) on extracellular concentrations of dopamine (DA) 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT), norepinephrine (NE) and DOPAC/DA ratio in intact, 6-hydroxydopamine (6-OHDA)-lesioned, DSP4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzyl-amine hydrochloride)-lesioned and reserpine-treated rats. The results revealed high basal DA (0.735+/-0.05 fmol/microl), DOPAC (195.93+/-20.18 fmol/microl) and NE (0.585+/-0.01 fmol/microl), low 5-HT (0.334+/-0.032 fmol/microl) and high DOPAC/DA ratio (265.11+/-20.73) in intact cACC. 6-OHDA alone (8 microg/2 microl) depleted DA (-66%), DOPAC (-65%), and NE (-62%). On the other hand, in desipramine (DMI)-pretreated rats, 6-OHDA induced a large depletion of DA (-94%), DOPAC (-97%) and reduced DOPAC/DA ratio (-73%), but increased NE to 142% of intact and 369% of 6-OHDA-lesioned rats. DSP4 (50 mg/kg) decreased NE (-97%), DOPAC (-75%) and DOPAC/DA ratio (-69%). Reserpine (5 mg/kg s.c.) significantly decreased DOPAC (-84%), DOPAC/DA ratio (-81%), 5-HT (-69%) and NE (-86%), but nonsignificantly increased DA. In the intact rats, MK-801 did not change DA, but increased DOPAC and DOPAC/DA ratio. In 6-OHDA-lesioned rats, MK-801 increased DA, whereas in 6-OHDA+DMI rats MK-801 additionally increased DOPAC and DOPAC/DA ratio. DSP4 and reserpine reduced the ability of MK-801 to increase DOPAC and DOPAC/DA ratio. MK-801 did not change NE concentration in dialysates collected from intact rats, but increased that from 6-OHDA+DMI-lesioned rats. In DSP4-lesioned and reserpine-treated rats, MK-801 increased NE but to a level lower than that observed in the intact rats. These results suggest that systemic administration of a low dose of MK-801, which induces profound locomotor stimulation without stereotypy, increases DOPAC and DOPAC/DA ratio in the cACC of intact rats, whereas it additionally increases the depleted DA and NE concentrations especially in 6-OHDA-lesioned rats pretreated with DMI.
3,4-Dihydroxyphenylacetic Acid↗
Selective and long-term learning impairment following neonatal hypoxic-ischemic brain insult in rats.
We examined four different learning and memory tasks in rats which had been subjected to left carotid artery ligation followed by 2 h hypoxia (8% oxygen) when they were 7 days old. The examination began on the 4th week after insult and continued to 18 weeks post-insult. Compared with the control group, the hypoxic-ischemic group showed significant learning impairments in choice reaction time tasks relating to the attention process, and in plus-maze tasks and water maze tasks which examine long-term reference memory. In eight-arm radial maze tasks representing both short-term working memory and long-term reference memory, inferiority of the hypoxic-ischemic group was transient. Results of the sensorimotor test were normal in the hypoxic-ischemic group although slight flexion and twisting in the right forelimb was observed in 30% of the hypoxic-ischemic group when suspended by the tail. These abnormalities did not affect the results of learning tests. Findings of the study indicate that left-side brain damage produced by hypoxia-ischemia at 7 days of age resulted in selective and long-lasting learning and memory impairment.
Animals↗
Involvement of anion exchange in the hypoxia/reoxygenation-induced changes in pH(i) and.
The involvement of Cl(-)/HCO(3)(-) exchange in hypoxia/reoxygenation-induced changes in pH(i) and Ca(2+) concentration ([Ca(2+)](i)) was examined in rat ventricular myocytes. During 10-min hypoxia, the initial pH(i) (7.21+/-0.04) fell to below 6.8. Subsequent reperfusion with reoxygenated buffer returned this acidic pH(i) to the neutral range with increases in [Ca(2+)](i). These responses were reduced by the removal of Cl(-) or HCO(3)(-) and by the addition of anion exchange inhibitors, SITS (4-acetamido-4'isothiocyanato-stilbene-2,2'disulfonic acid) and DIDS (4,4'-diisothiocyano-stilbene-2,2'-disulfonic acid), while inhibitors for the Cl(-) channel and Na(+)/K(+)/2Cl(-) cotransport were without effects. The hypoxia-induced acidification was attenuated by protein kinase C inhibitors, calphostin C and chelerythrine, but not by a protein kinase A inhibitor, KT5720. Under normoxic condition, protein kinase C activation induced a SITS-sensitive acidification. Furthermore, in electrically driven rat papillary muscle, SITS and DIDS improved the recovery of developed tension during the reoxygenation. These results suggest that the hypoxia-induced decrease in pH(i) is mediated at least in part by anion exchange stimulation through protein kinase C activation, and this exchange takes part in the reoxygenation-induced Ca(2+) overload as well as contractile dysfunction.
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
Treatment modalities for oral verrucous carcinomas and their outcomes: contribution of radiotherapy and chemotherapy.
BACKGROUND: This clinical study focused, firstly, on the results of treatment and, secondly, on the anaplastic transformation, of oral verrucous carcinomas (OVCs) diagnosed and treated from 1981 to 1997 at the Department of Oral and Maxillofacial Surgery at Shimane Medical University Hospital. METHODS: We analyzed the treatment modalities and outcomes for 15 patients with OVC. RESULTS: Excluding the results for 4 palliatively treated patients, the disease-free survival rates of the patients after the initial treatments, were 82% at 5 years and 66% at 10 years; for all 15 patients, these rates were 57% and 46%, respectively. Surgery alone and surgery combined with other treatments (such as radiotherapy and chemotherapy) appeared to yield disease-free survival rates to those achieved superior with other treatments whether single or combined; (78% vs 33% for 5-year disease-free survival; 52% vs 33% for 10-year disease-free survival); however, the difference was not significant (P = 0.47). Well differentiated squamous cell carcinomas (W-SCCs) (n = 5) as well as spindle cell carcinoma (n = 1) were found in subsequent operative or biopsy specimens. CONCLUSION: Surgery was the most reliable treatment method for OVC; however, radiotherapy combined with chemotherapy was the next most preferable treatment when surgery was not undertaken. We also found that highly malignant transformation (anaplastic transformation) occasionally occurred during treatments for OVC.
Aged↗
Curvature elasticity of multilamellar lipid bilayers close to the chain-melting transition.
We directly measured curvature elasticity of dipalmitoylphosphatidylcholine multilamellar bilayers close to the chain-melting transition using the method of electric-field-induced bending deformation of the cylindrical tubes. The result shows that the bending modulus, kappa(c), decreases remarkably at temperatures close to the melting transition temperature. This reflects a softening of the bilayer resulted from the area fluctuations as predicted theoretically. However, the decrease of kappa(c) near the transition is far smaller than that predicted. This is due to the experimental method and the narrow transition width of the multilamellar bilayers. Nevertheless, the result obtained gives direct evidence of the kappa(c) reduction predicted for multilamellar membranes in the transition regime. Below about 41 degrees C, almost of all cylindrical tubes cannot response to the electric field, indicating a very large bending rigidity.
1,2-Dipalmitoylphosphatidylcholine↗