Transplantation of feline islets of Langerhans in the subretinal space of cat eyes.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
T Maeno
Publications and source records attributed to T Maeno.
Effects of carbamazepine on nerve activity and transmitter release in neuroblastoma-glioma hybrid cells and the frog neuromuscular junction.
Effects of the antiepileptic drug carbamazepine on nerve action potential and transmitter release in mouse neuroblastoma-glioma hybrid cells (NG108-15) and the frog neuromuscular junction were studied. Carbamazepine within a concentration range of 0.1-0.5 mmol/L reduced the peak height of the action potential of the NG108-15 cells, whereas the membrane potential and membrane resistance were unaffected. Voltage clamp revealed that the decrease in the action was due to the blockage of the Na+, delayed K+ and transient Ca2+ currents. Carbamazepine did not affect Ca(2+)-activated and A type K+ currents and long-lasting Ca2+ current. In the frog neuromuscular junction, carbamazepine decreased the mean quantal content by a parallel shift in the frequency augmentation-potentiation (FAP) relation. It is concluded that carbamazepine blocks the voltage-dependent Na+, delayed K+, and transient Ca2+ currents and quantal transmitter release through a decrease of nerve excitation.
Action Potentials↗
[The outcome of patients with mediastinal tumors detected by mass screening versus the outcome of those initially presentating with symptoms].
Forty seven patients with mediastinal tumors, who were diagnosed between 1976 and 1996 at Tsukuba University Hospital, were evaluated according to the circumstances surrounding their initial consultations. The outcome of 19 patients (40.4%) whose tumors were detected by mass screening was compared with the outcome of 20 patients (42.6%) whose tumors were detected after presenting with symptoms. In the mass screening group, only 21% of the patients had a malignant neoplasm, whereas 75% of patients in the symptomatic group had a malignant neoplasm (p = 0.0008). Patients in the screening group had a shorter hospital stay than those in the symptomatic group (60.5 vs. 118. 1days; p = 0.0022). In patients with thymomas, in the mass screening all patients group were at stage I or II. Only 20% of the lesions in symptomatic patients were at stage I or II (p < 0.0001). Based on the results of this study, we believe that the early detection of mediastinal tumors via mass screening might have clinical significance.
Adolescent↗
[A case of Sairei-to-induced pneumonitis diagnosed by lymphocyte stimulation test of bronchoalveolar lavage fluid].
A 51-year-old woman was admitted with fever, cough and dyspnea. She had been taking Sairei-to, a traditional Chinese medicine, for 2 months. On admission, chest X-ray revealed a ground-glass appearance in the lung fields bilaterally and serum LDH was elevated. A differential cell count of the bronchoalveolar lavage fluid (BALF) showed that lymphocytes were increased, with a decreased ratio of CD4/CD8 cells. A lymphocyte stimulation test (LST) for Sairei-to using the lymphocytes in BALF was a positive, although a test of peripheral blood was negative. Sairei-to-induced pneumonitis was diagnosed based on the clinical course, laboratory findings, BALF cell analysis and LST of BALF. Only 4 cases of pneumonitis due to Sairei-to have been reported. This case suggests that LST of BALF is useful for diagnosing drug-induced pneumonitis.
Bronchoalveolar Lavage Fluid↗
Surgical removal of submacular hemorrhage using tissue plasminogen activator and perfluorocarbon liquid.
PURPOSE: To assess the result of surgical removal of submacular hemorrhage by using tissue plasminogen activator and perfluorocarbon liquid. METHODS: In 22 consecutive patients (22 eyes), subretinal hemorrhage associated with age-related macular degeneration, which involved the fovea and completely obscured the choroidal vascular pattern, was treated by pars plana vitrectomy. The hemorrhages were liquefied with tissue plasminogen activator, squeezed into the vitreous cavity with perfluorocarbon liquid, and then evacuated. RESULTS: Efficacy of the procedure was judged by the best postoperative corrected visual acuity, which was 20/100 or better in 16 eyes (73%). Submacular hemorrhage recurred in four (18%) eyes, epiretinal membrane formed in three (14%) eyes, and retinal detachment occurred in three (14%) eyes. Best-corrected final visual acuity was improved postoperatively in 18 (82%) of the 22 eyes, unchanged in three (14%) eyes, and decreased in one (5%) eye, final visual acuity was 20/200 or better in 15 eyes (68%) and limited in other eyes by subretinal hemorrhage of greater than 30 days' duration or subfoveal neovascularizations. CONCLUSIONS: Use of tissue plasminogen activator and perfluorocarbon liquid in surgical removal of submacular hemorrhage may improve the outcome of surgery by reducing surgically induced retinal damage.
Aged↗
[Visual functional changes in idiopathic macular holes treated by vitrectomy].
We evaluated visual functional measurements, visual acuity, central retinal sensitivity in a Humphrey field analyzer, and binocular function in Stereotest, Amsler grid testing, of 51 idiopathic macular holes before and after vitrectomy. In 36 of 51 eyes (71%) where the macular hole was closed after vitrectomy, there were improvements in all visual functional measurements postoperatively. The eyes in which the macular hole was closed had significantly better visual acuity before vitrectomy than those in which the hole was not closed. In 16 of 51 eyes that had visual acuity of less than 20/200 preoperatively, central retinal sensitivity before vitrectomy was higher in the eyes where the macular hole was closed than in those in which it was not closed. These measurements are useful for evaluation of visual functional improvements after vitrectomy and can help to choose candidates for macular hole surgery.
Adult↗
Modification of frequency augmentation-potentiation by GTP gamma S in the frog neuromuscular junction.
The effect of modifiers of guanine nucleotide-binding proteins (G proteins) on the frequency augmentation-potentiation of transmitter release were studied in the frog neuromuscular junction. Using Genetransfer as a carrier the mean quantal content of the endplate potential increased by penetration of GTP gamma S into the presynaptic nerve terminal. Neither GTP gamma S alone nor carrier alone had any effect. The relationship of log (mean quantal content) versus stimulation frequency changed from a single linear to a dual linear function, suggesting that the immediately releasable pool was modified. GDP beta S + carrier also had similar effects, but was less potent. Aluminium fluoride was without effect. Extracellularly recorded presynaptic nerve action potentials remained unchanged with GTP gamma S + carrier. Also, GTP gamma S + carrier did not affect the action potential nor the cytosolic Ca2+ concentration in differentiated NG108-15 hybrid cells. It is suggested that some smg-type G protein-dependent processes are involved in determining frequency augmentation-potentiation.
Action Potentials↗
Release of arachidonic acid via Ca2+ increase stimulated by pyrophosphonucleotides and bradykinin in mammary tumour cells.
The relationship between the increase of intracellular Ca2+ and the release of arachidonic acid by bradykinin and pyrophosphonucleotides was studied in cultured mammary tumour cells, MMT060562. Bradykinin, ATP, UTP and UDP induced an increase of intracellular Ca2+ and the release of arachidonic acid from phospholipids into the extracellular fluid. Release of arachidonic acid was also induced by the application of the Ca2+ ionophore, A23187. Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist. It is suggested that the increase in cytosolic Ca(2+)-induced release of arachidonic acid occurs through activation of calmodulin-dependent phospholipase A2.
Adenosine Triphosphate↗
Spontaneous aortic thrombosis in a neonate with multiple thrombi in the main branches of the abdominal aorta.
Spontaneous aortic thrombosis in the neonate is a rare entity with a high mortality rate. The present patient, who was diagnosed after showing haematuria and cyanosis, underwent aortic thrombectomy with a Fogarty catheter through a left thoracotomy, but died of sepsis, disseminated intravascular coagulation and multiple organ failure. Autopsy revealed multiple residual thrombi in the main branches of the abdominal aorta and necrosis of the abdominal organs despite a patent thoracoabdominal aorta. In patients with no blood flow in the main branches of the abdominal aorta on preoperative examination, removal of thrombi, including those in the main branches of the abdominal aorta, might be performed in a single, early and aggressive procedure.
Aorta, Abdominal↗
Effects of inhibitors of ouabain-sensitive Na+, K(+)-ATPase and Li+ ions on the neuromuscular transmission of the frog.
The effect of blockade of ouabain-sensitive alpha 2 and alpha 3 (neural type) isozymes of Na+, K(+)-ATPase was investigated on frog neuromuscular preparations by recording the frequency augmentation-potentiation (FAP) of the endplate potential, an electrophysiological and neuropharmacological technique to analyze the drug actions on the release process of the readily releasable transmitter quanta. Erythrosin B, which was thought to selectively inhibit the neural type Na+, K(+)-ATPase, pivoted the log-linear FAP relation counterclockwise without altering the intercept on the ordinate. Chlormadinone had a similar action. An increase in the concentration of extracellular K+ ions pivoted the FAP relation clockwise with a concomitant upward shift of the intercept on the ordinate, and low K+ Ringer's solution produced an inverse effect. In contrast, Li+ ions shifted the FAP relation upwards dose-dependently leaving its slope unchanged. Cinnarizine, a blocker for inositol-1,4,5-trisphosphate-induced Ca2+ release, and 5,5'-dimethyl-1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid, a specific intracellular Ca2+ chelator, significantly antagonized the potentiating action of Li+. The ouabain-sensitive neural type Na+, K(+)-ATPase isozyme, which is abundant in neural tissues, seems to play an important role in stimulation frequency-dependent modulation of the quantal transmitter release such as FAP.
Adrenal Cortex Hormones↗
Chemical modification by maleimide of toxic and nontoxic ouabain actions on neuromuscular transmission in the frog.
A dual action of ouabain on the Mg(2+)-blocked frog neuromuscular transmission was studied in two different experimental procedures by measuring the mean quantal content (m) of endplate potentials evoked during repetitive nerve stimulation. The nontoxic action of low-dose (1 microM) ouabain was observed as a counterclockwise pivoting of the linear stimulation frequency versus the log m relation, termed frequency augmentation-potentiation (FAP), whereas the toxic effect of higher doses (> or = 10 microM) of ouabain was recorded as a slow exponential increase in m. Since neural Na+,K(+)-ATPase consists of two or three isoforms, the nontoxic action of low-dose ouabain was anticipated to be a consequence of the selective inhibition of ouabain-sensitive alpha(+) (alpha 2 and alpha 3 or neural type) Na+,K(+)-ATPase activity. Such a possibility was assessed by applying epsilon-maleimidocaproic acid (MCA), a membrane-impermeant sulfhydryl reagent. MCA 15 microM was found in the present study to suppress the nontoxic effect of ouabain without altering the toxic effect. The results strongly suggest that the toxic and nontoxic actions of ouabain are the result of actions on different entities. The ouabain-sensitive neural type Na+,K(+)-ATPase, which is abundant in neural tissues, seems to play an important role in modulation of transmitter release observable as FAP.
Animals↗
Toxic and nontoxic effects of ouabain on the transmitter release from frog motor nerve terminals.
Toxic and nontoxic effects of ouabain were investigated on frog neuromuscular preparation by measuring the mean quantal content of endplate potentials elicited during repetitive nerve stimulation. In the untreated normal muscles, application of 10 microM ouabain gave rise to a slow exponential increase in the transmitter release (toxic ouabain effect) with a certain delay. This delay was increased with either 100 microM amiloride, a Na(+)-Ca2+ exchange blocker, or the intracellular loading of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a specific intracellular Ca2+ chelator. Measurements of frequency augmentation-potentiation (FAP) revealed a specific nontoxic effect of ouabain: 1 microM ouabain pivoted the long-linear FAP relation counter-clockwise without altering the intercept on the ordinate. Contrary to their action in the toxic effect, both 100 microM amiloride and the intracellular loading of BAPTA failed to counteract the nontoxic effect of 1 microM ouabain. The present results suggest that the toxic and nontoxic effects of ouabain are of different entities. The ouabain-sensitive subtype of Na+,K(+)-ATPase, which is abundant in neural tissues, seems to play a specific role in the process of nontoxic potentiation of transmitter release.
Amiloride↗
[Effects of the nitric oxide donor SIN-1 on the membrane potential of mouse neuroblastoma-rat glioma hybrid cells].
The effect of the nitric oxide donor SIN-1 on the membrane potential of cultured mouse neuroblastoma-rat glioma hybrid NG108-15 cells was investigated using the whole cell patch method. It has been reported that neurite formation can be induced in NG108-15 cells by adding of dibutyryl cyclic AMP to the culture medium. Using this system we found that SIN-1 has a selective inhibitory effect on the membrane potential of the calcium current which is concentration-dependent in the 1 mu M-100 microM range. This effect was transient and reversible, the same as seen with the calcium channel blocker nilvadipine at concentrations of 10 microM to 10 microM. At higher concentrations, ranging from 500 microM to 1 mM, however, SIN-1 also caused prolonged inhibition of the membrane potential of the sodium current. However, this effect was also reversible. These findings suggest that SIN-1 has a reversible inhibitory action on the membrane potentials of neurons.
Animals↗
[Glial tumor cell proliferation and immune response in the brain].
The mechanism of glial tumor cell proliferation and the immune response to glioma cells in the brain were examined both in vitro and in vivo experimental systems, using mouse malignant glioma cell line, 203-glioma. A fura-2 fluorescence image showed marked rise in the intracellular calcium ion concentration in mechanically stimulated single cells. The increased calcium spread to adjacent cells, probably due to some stimulating factor released from cells. Dye microinjection revealed no gap junction between cells. Antagonists of voltage-dependent calcium channels did not act on the calcium response. These suggest that calcium signaling in the glioma cells may be mediated via a membrane receptor but not through a gap junction. Depletion of extracellular calcium ion and addition of intracellular calcium blocker demonstrated that calcium signaling in stimulated cells may be related to both an influx of extracellular calcium and a redistribution of intracellular calcium from internal stores, whereas calcium transmission to adjacent cells may involve calcium influx alone. The splenic cytotoxic T lymphocyte (CTL) activity in intracerebral tumor-bearing hosts increased with a peak 2 weeks after tumor cell inoculation, but rapidly decreased concurrently with increased intracranial pressure. The major histocompatibility complex, MHC, class I antigen expression on tumor cells grafted intracerebrally was found to enhance markedly, resulting in an increase in susceptibility to CTL. It was suggested that there may be a positive correlation between the cell surface MHC class I antigen expression and sensitivity to CTL in glioma cells.
Animals↗
Inhibitory effect of vasoactive intestinal peptide (VIP) on phagocytosis in mouse peritoneal macrophages.
The effect of VIP on phagocytosis in peritoneal macrophages was examined by means of flow cytometry (FCM). This assay revealed that VIP suppressed phagocytosis in a dose-dependent manner. VIP(1-12) did not suppress phagocytosis. VIP(10-28) was more suppressive than VIP(1-28). A known VIP-antagonist (N-Ac-Tyr1,D-Phe2)-growth hormone-releasing factor (GRF) (1-29)-NH2 suppressed phagocytosis less than VIP. Control phagocytosis was partially suppressed in Ca(2+)-free solution. Phagocytosis was suppressed by VIP further in Ca(2+)-free solution than in the normal solution. Phagocytosis was suppressed in a known phosphodiesterase inhibitor IBMX-containing solution. The degree of suppression by VIP was the same in the presence or the absence of IBMX. These results suggest that VIP suppresses extracellular Ca(2+)-dependent and -independent phagocytosis, that the C-terminal fragment of VIP is essential for VIP action, that the suppression is mediated by cAMP and that the inhibition of macrophage phagocytosis by VIP is one of the mechanisms which modulates immune responses by the nervous system.
1-Methyl-3-isobutylxanthine↗
Induction of differentiation by radiation and hyperthermia in neuroblastoma-glioma hybrid cells.
The effects of either radiation or hyperthermia on the differentiation potential of NG108-15, a neuroblastoma-glioma hybrid cell line, were studied. After radiation and hyperthermia, the outgrowth of neurites from NG108-15 cells was potentiated, and polarizing current and voltage pulses induced a distinct action potential and a diphasic (inward following outward) current, respectively. An increase in the specific activity of acetylcholinesterase was also observed. In addition, both treatments induced an elevation of the concentration of intracellular calcium in some cells. The increase in intracellular calcium concentration caused by applying the calcium ionophore, A23187, induced differentiation. It is suggested that both the radiation- and the hyperthermia-induced increases of electrical excitability and acetylcholinesterase activity may have originated from an increase in intracellular Ca2+ concentration.
Acetylcholinesterase↗
A flow cytometric assay reveals an enhancement of phagocytosis by platelet activating factor in murine peritoneal macrophages.
Phagocytosis of fluorescein isothiocyanate-labeled latex beads by peritoneal macrophages from thioglycollate-stimulated mice was examined in vitro by means of flow cytometry. This assay revealed that platelet activating factor (PAF), a known inflammatory mediator, enhanced the phagocytosis in a dose-dependent manner. The enhancement was completely suppressed by a PAF antagonist, Y-24180, and partly suppressed by another antagonist, CV-3988. The phagocytosis of both nonstimulated and PAF-stimulated macrophages was suppressed in Ca(2+)-free ethylene glycol bis(beta-aminoethyl ether) N,N'-tetraacetic acid-containing solution, but the phagocytosis was enhanced by PAF even in this solution. These results suggest that phagocytosis by macrophages is enhanced by PAF in allergic and inflammatory reactions.
Animals↗
The increase in the intracellular Ca2+ concentration induced by mechanical stimulation is propagated via release of pyrophosphorylated nucleotides in mammary epithelial cells.
Mechanical stimulation of one mammary tumor cell in culture induced an increase in its intracellular calcium concentration which spread to surrounding cells. The increase in calcium can also be induced by addition of a solution in which cultured mammary tumor cells were stimulated by repeated pipetting (solution after pipetting cells, SAPC). The activity of the SAPC was completely abolished by treatment with snake venom phosphodiesterase or pyrophosphatase. Uridine triphosphate (UTP), uridine diphosphate (UDP) and ATP (1 microM each) were detected in the SAPC, whereas 5'-UMP and 5'-AMP were produced by phosphodiesterase digestion. A mixture of UTP, UDP and ATP (1 microM each) elicited a calcium response which was comparable to that induced by SAPC, while UTP, UDP or ATP alone at 1 microM elicited a small increase in calcium concentration in mammary tumor cells. Suramin, a competitive antagonist of P2 purinoceptors, diminished the spreading of the calcium wave induced by mechanical stimulation. It also blocked the responses to SAPC, UTP, UDP and ATP. These findings suggest that the mechanical stimulation results in the release of UTP, UDP and ATP into the extracellular space which mediates induction of the spreading calcium response via P2U-type purinoceptors.
Adenosine Triphosphate↗