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Biomedical subjects

A Mori

Publications and source records attributed to A Mori.

At least 19 recordsLinked to original sources

Mizoroki-Heck type reaction of organoboron reagents with alkenes and alkynes. A Pd(II)-catalyzed pathway with Cu(OAc)2 as an oxidant.

[reaction: see text]. In contrast to the Pd(0)-catalyzed mechanism by Uemura, Mizoroki-Heck type reaction of boronic acids is found to proceed under a Pd(II)-mediated pathway using a catalytic amount of Pd(OAc)2 in the presence of Cu(OAc)2 as an oxidant. Treatment of a variety of alkenes with boronic acids, boronates, and sodium tetraphenylborate furnishes beta-arylated and alkenylated products in good to excellent yields. The reactions with norbornene, norbornadiene, and diphenylacetylene are also performed to give 1:2 or 2:1 coupling products.

Journal Article↗

Mouse macrophage metalloelastase gene delivery by HVJ-cationic liposomes in experimental antiangiogenic gene therapy for murine CT-26 colon cancer.

We previously demonstrated that gene replacement of mouse macrophage metalloelastase (MME) into murine melanoma cells that grow rapidly and are MME deficient suppresses the primary tumor growth in vivo by halting angiogenesis. The aim of the present study was to evaluate the effectiveness of gene therapy against cancer using a cDNA-encoding MME gene. In a subcutaneous tumor model of CT-26 mouse colon cancer cells that are MME deficient, syngeneic mice repetitively treated with direct injections into the tumors of MME- hemagglutinating virus of Japan (HVJ), a type of HVJ-cationic liposome encapsulating a plasmid expressing MME, developed smaller tumors (210 +/- 47.2 mm(3) versus 925 +/- 156 mm(3) mean +/- SEM; p = 0.0004) with fewer microvessels (10.25 +/- 1.03 vs. 17.25 +/- 2.14; p = 0.03) than control mice. TUNEL staining revealed a significant increase of apoptotic cells in the MME-HVJ liposomes-treated tumors compared with control tumors. MME was effectively expressed in the s.c. tumors treated with MME-HVJ liposomes, inducing angiostatin generation in those tumors, as demonstrated by Western blot analysis. In conclusion, our study demonstrated that repeated in vivo transduction of the MME gene directly into the tumors using HVJ-cationic liposomes suppressed the tumor growth by an antiangiogenic mechanism, providing, then, a feasible strategy for gene therapy of cancer.

Angiostatins↗

Two types of movement-related cortical potentials preceding wrist extension in humans.

We compared the occurrence patterns of movement-related cortical potentials (MRCPs) preceding wrist extension in athletes (kendoists and gymnasts) and non-athletes. The MRCPs of the non-athletes started approximately 1.5 s before the EMG onset of wrist extension. In the athletes, the duration of the MRCPs was shorter and the amplitudes of early component (Bereitschaftspotential) were smaller than in the non-athletes. The MRCPs in the athletes started approximately 400 ms before the onset of wrist extension and increased rapidly. In topographical maps, MRCPs of the athletes were localized markedly on the contralateral motor area (C3) compared with the non-athletes. In the present study, the duration of MRCPs was classified into two types.

Adolescent↗

Regioselective oxygenations of s-trans dienes, silyl dienol ethers (SDEs), by triphenyl phosphite ozonide (TPPO) and its mechanistic study.

The direct oxygenation of s-trans dienes, silyl dienol ethers (SDEs) 2, by triphenyl phosphite ozonide (TPPO) has been examined in detail. The regioselective oxygenation was found to give hydroperoxide 3, alcohol 4, ketone 5, dimer 6, and peroxy phosphate 7 with concomitant formation of triphenyl phosphate 8 and diphenyl trimethylsilyl phosphate 10. The formation of peroxy phosphate 7 was found for the first time in TPPO oxygenation reactions. The low temperature (31)P and (1)H NMR spectroscopic analyses proved the direct reaction of SDEs with TPPO without generation of singlet oxygen. The formation of the oxygenated products 3-7 is reasonably explained by the intervention of the zwitterion ZI, which can be formed by the nucleophilic attack of SDE to the central oxygen of the ozonide. The regioselective attack of SDE to the central oxygen of the ozonide was supported by the quantum chemical calculation (B3LYP/6-31G).

Journal Article↗

5-Cyanotropolone and 5-nitrotropolone.

The title compounds, 4-hydroxy-5-oxo-1,3,6-cycloheptatriene-1-carbonitrile, C(8)H(5)NO(2), (I), and 2-hydroxy-5-nitro-2,4,6-cycloheptatrien-1-one, C(7)H(5)NO(4), (II), have intra- and intermolecular hydrogen bonds. The structure of (II) contains two crystallographically independent molecules, (IIa) and (IIb). An intermolecular pi-pi interaction and an intermolecular NO(2).pi-pi interaction are present in (I) and (II), respectively.

Journal Article↗

Adenosine A(2A) receptor enhances GABA(A)-mediated IPSCs in the rat globus pallidus.

1. The actions of adenosine A(2A) receptor agonists were examined on GABAergic synaptic transmission in the globus pallidus (GP) in rat brain slices using whole-cell patch-clamp recording. GP neurones were characterized into two major groups, type I and type II, according to the degree of time-dependent hyperpolarization-activated inward rectification and the size of input resistance. 2. The A(2A) receptor agonist 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamido- adenosine (CGS21680; 0.3-3 microM) enhanced IPSCs evoked by stimulation within the GP. The actions of CGS21680 were blocked by the A(2A) antagonists (E)-8-(3,4-dimethoxystyryl)-1,3-dipropyl-7-methylxanthine (KF17837) and 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM241385). 3. The CGS21680-induced increase in IPSCs was associated with a reduction in paired-pulse facilitation. CGS21680 (0.3 microM) increased the frequency of miniature IPSCs (mIPSCs) without affecting mIPSC amplitude. These observations demonstrated that the enhancement of IPSCs in the GP was attributable to presynaptic, but not postsynaptic, A(2A) receptors. 4. The results suggest that A(2A) receptors in the GP serve to inhibit GP neuronal activity, thereby disinhibiting subthalamic nucleus neurone activity. Thus, the A(2A) receptor-mediated presynaptic regulation in the GP, together with the A(2A) receptor-mediated intrastriatal presynaptic control of GABAergic neurotransmission described previously, may play a crucial role in controlling the neuronal functions of basal ganglia. This A(2A) receptor-mediated presynaptic dual control in the striatopallidal pathway could also afford the mode of action of A(2A) antagonists for ameliorating the symptoms of Parkinson's disease in an animal model.

Animals↗

Enhancement of arachidonic acid release and prostaglandin F(2alpha) formation by Na3VO4 in PC12 cells and GH3 cells.

Both activation of phospholipase A2 causing arachidonic acid release and tyrosine phosphorylation have been proposed to be involved in neuronal functions. Previously, we reported that orthovanadate (Na3VO4), an inhibitor of tyrosine phosphatases, stimulated tyrosine phosphorylation in proteins and enhanced Ca2+-induced noradrenaline release in rat pheochromocytoma PC12 cells. However, the role of tyrosine phosphorylation on phospholipase A2 activity and/or arachidonic acid release in neuronal cells has not been well established. The effects of Na3VO4 on arachidonic acid release and prostaglandin F(2alpha) formation were investigated in two types of neuronal cell lines. In PC12 cells, addition of Na3VO4 stimulated [3H]arachidonic acid release and prostaglandin F(2alpha) formation in a concentration-dependent manner. Co-addition of 5 mM Na3VO4 enhanced ionomycin-stimulated [3H]arachidonic acid release. Na3VO4 also enhanced ionomycin-stimulated [3H]arachidonic acid release from GH3 cells, a clonal strain from rat anterior pituitary. These findings suggest that the tyrosine phosphorylation pathway regulates arachidonic acid release by phospholipase A2 and prostaglandin F(2alpha) formation in neuronal cells.

Animals↗

Human macrophage metalloelastase gene expression in colorectal carcinoma and its clinicopathologic significance.

BACKGROUND: Human macrophage metalloelastase (HME), also referred as matrix metalloproteinase 12, has been shown to convert plasminogen into angiostatin, an essential inhibitor of tumor angiogenesis. The current study was designed to investigate the association of HME mRNA expression with disease progression of in patients with colorectal carcinoma. METHODS: The expression of HME mRNA was quantified by Northern blot analysis in tumorous (T) and nontumorous (N) tissues obtained from 54 patients with primary colorectal carcinoma, and the ratio of these two tissue types was defined as the HME T/N ratio. The prognostic significance of this ratio after surgery, along with its correlation with disease progression and metastatic potential, was evaluated. The tissues also were subjected to in situ hybridization analysis for HME. The microvessel count after immunohistochemical staining of factor VIII was used to assess angiogenesis. RESULTS: The HME T/N ratio showed an inverse correlation with the depth of the intestinal wall invasion, the lymphatic invasion, and the vascular invasion. The patients with overexpression of HME mRNA (HME T/N ratio > 1.191) significantly demonstrated better survival compared with those patients who did not show overexpression of HME mRNA. In situ hybridization identified the colorectal carcinoma cells as mainly responsible for the signal shown in Northern blot analysis. A considerable but not statistically significant lower microvessel density (MVD) was observed in the patients with HME overexpression. CONCLUSIONS: These findings demonstrate that the HME gene plays an important role in the inhibition of tumor progression in patients with colorectal carcinoma and that its overexpression is correlated closely with a better prognosis.

Aged↗

Phencyclidine-induced discriminative stimulus is mediated via phencyclidine binding sites on the N-methyl-D-aspartate receptor-ion channel complex, not via sigma(1) receptors.

The effects of several N-methyl-D-aspartate (NMDA) receptor- and sigma receptor-related compounds on the discriminative stimulus effects of phencyclidine (PCP) were examined in rats trained to discriminate PCP (1.5 mg/kg, i.p.) from saline under a two-lever fixed ratio 20 schedule of food reinforcement. PCP produced a dose-dependent increase in PCP-appropriate responding. A non-competitive NMDA receptor antagonist, dizocilpine (0.2 mg/kg, i.p.) and a putative sigma(1) receptor agonist, (+)-SKF-10047 (10 mg/kg, i.p.) fully substituted for PCP in every rat tested. Neither a competitive NMDA receptor antagonist, CGS-19755 (0.1-3 mg/kg, i.p.), sigma(1) receptor agonist, (+)-pentazocine (10-30 mg/kg, i.p.) nor dextromethorphan (10-20 mg/kg, i.p.) produced PCP-like discriminative stimulus effects. The discriminative stimulus effects of PCP (1.5 mg/kg, i.p.), dizocilpine (0.2 mg/kg, i.p.) and (+)-SKF-10047 (10 mg/kg, i.p.) were significantly attenuated by CGS-19755 (1 mg/kg, i.p.), but not by sigma(1) receptor antagonist BMY-14802 (10 mg/kg, i.p.) and NE-100 (5 mg/kg, i.p.). These results suggest that the discriminative stimulus effects of PCP are predominantly mediated via PCP binding sites on the NMDA receptor-ion channel complex, not via sigma(1) receptors. In addition, the PCP-like discriminative stimulus effects of (+)-SKF-10047 were demonstrated to be mediated via PCP binding sites.

Animals↗

Dynamics of antigen-specific helper T cells at the initiation of airway eosinophilic inflammation.

Bronchial asthma is characterized by chronic eosinophilic inflammation of the bronchial mucosa in which Th2 cells play crucial roles. Ovalbumin-reactive Th2 clones were labeled with a fluorescent-probe then infused into unprimed mice to elucidate the dynamics of antigen-specific T cells involved in allergic inflammation. Infiltration of not only labeled antigen-specific T cells, but also unlabeled nonspecific CD4(+) T cells into the bronchial mucosa following inhaled antigen challenge was detectable under confocal microscopy and flow cytometry. Accordingly, labeled T cells in the spleen were decreased, whereas those in hilar lymph nodes were increased upon antigen challenge. Approximately 45% of antigen-specific T cells that migrated into the lungs bore CD25, while another early activation marker, CD69, was expressed on 80% of the migrated T cells. Accordingly, antigen challenge to the mice induced in situ proliferation of antigen-specific T cells as well as bronchial epithelial cells in the lungs. Expression of vascular cell adhesion molecule (VCAM)-1, but not intercellular adhesion molecule (ICAM)-1, on the vascular endothelium in the lungs was enhanced following antigen challenge. Nevertheless, treatment with anti-VCAM-1 antibody, and also anti-ICAM-1 antibody strongly suppressed the accumulation of T cells, suggesting that both VCAM-1 and ICAM-1 are essential for antigen-stimulated T cell mobilization into peripheral tissues. Our current study visualized the kinetics and the mechanism of antigen-specific T cell migration in response to local challenge with a protein antigen.

Adoptive Transfer↗

Aortic subannular left ventricular aneurysm in a patient of Asian ancestry.

An asymptomatic 50-year-old Japanese man was diagnosed with an aortic subannular left ventricular aneurysm during a routine physical checkup. Operative findings showed the subaortic aneurysm had developed beneath the noncoronary cusp of the aortic valve and expanded into the epicardium between the aortic root and left atrium. The operation involved patch closure of the orifice of the annular subaortic aneurysm, aortic valvuloplasty, and plication of the dilated ascending aorta.

Aortic Aneurysm↗

Avascular necrosis in the femoral head secondary to bone marrow infarction in a patient with graft-versus-host disease after unrelated bone marrow transplantation.

We previously reported a case of bone marrow infarction attributable to acute graft-versus-host disease (GVHD) in a patient with acute lymphoblastic leukemia after unrelated bone marrow transplantation (BMT). Although the bone marrow infarction-induced arthralgia in this patient improved, severe arthralgia appeared again with exacerbation of chronic GVHD, and the arthralgia was strongly correlated with the clinical course of chronic GVHD, i.e., the course of symptoms such as dermal and hepatic GVHD and ocular dryness. Finally, the patient developed avascular necrosis (AVN) in the right femoral head. Serum interleukin (IL)-6 and IL-10 levels were high at the onset of arthralgia but low during remission, and levels of interferon-gamma were undetectable throughout the period of arthralgia. Based on the clinical course and these data, chronic GVHD was thought to have been the major cause of the AVN. Since IL-10 antagonizes various other cytokines that induce GVHD, the increase in IL-10 might have inhibited the development of GVHD.

Adult↗

Fetal aortic blood flow assessment from the relationship between fetal aortic diameter pulse and flow velocity waveforms during fetal development.

BACKGROUND: Blood flow is calculated from mean velocity across the vessel and its cross-sectional area and is related to the fetal growth. AIM: To investigate the relationship between diameter pulse waveform (DPW) and flow velocity waveform (FVW) in the fetal descending aorta during fetal development. STUDY DESIGN: Doppler ultrasound and a phase-locked loop echo tracking system were used to measure the FVW and DPW in the fetal descending aorta, respectively. SUBJECTS: We studied 137 normal-growth fetuses (normal group, 20-40 weeks) and 51 fetuses with high umbilical artery pulsatility index (umbilical placental insufficiency, UPI group, 26-40 weeks). OUTCOME MEASURES: We measured the systolic (Sd), diastolic (Dd) diameters, time diameter integral (TDI) and time velocity integral (TVI) and then calculated the TVI x TDI and TVI to TDI ratio. RESULTS: Normal fetal growth was associated with an increase in Sd, Dd, pulse amplitude, TVI, TDI and TVI x TDI. The FVW began to resemble the DPW with decreasing downstream resistance produced by growth of the placenta. The TVI was increased relative to the TDI. The differences in Sd, Dd, TDI and TVI x TDI between the normal and UPI groups were not significant. The TVI was decreased relative to the TDI. There was a decrease in the TVI as a ratio of the TDI. The Dd per unit fetal weight was high in the compromised fetuses. Fetal outcome was examined in relation to the TVI to TDI ratio. Those with a low ratio (below 10th centile) exhibited significantly more adverse indices of fetal outcome. CONCLUSIONS: In fetal compromise there is an increase in diastolic pressure in association with high placental resistance, which causes a major increase in afterload. The efficient circulation associated with fetal growth might be represented by an increase in the ratio of the TVI to the TDI (an index of efficient circulation) when these waveform shapes resemble each other.

Adult↗

Plasma growth hormone (GH) responses after administration of the peptidergic GH secretagogue KP102 into the oral cavity, rumen, abomasum and duodenum in adult goats.

The study was performed to determine whether orally administered KP102 (also known as GHRP-2) stimulates GH release in adult goats, and how the orally administered KP102 passes through the digestive tract and stimulates GH release in ruminant animals. Five mg/kg body weight (BW) of KP102 dissolved in 9 ml of saline were administered into the oral cavity, rumen, omasum and duodenum of adult goats, and GH release after administration of KP102 was examined. The GH levels were significantly elevated at 20 min after administration of KP102 into the oral cavity, and plasma concentrations of GH remained significantly elevated until 60 min (P < 0.05). The GH levels after administration of KP102 into the abomasum were variable. However, the GH level tended to increase within 30 min after administration, and were significantly higher than those of controls after 120 to 150 min (P < 0.05). The GH levels after administration of KP102 into the duodenum were significantly elevated at 40 min after administration, and plasma concentrations of GH remained significantly elevated until 140 min (P < 0.05). The administration of KP102 into the rumen failed to stimulate GH release. The GH response curves (AUC) produced after administration of KP102 into the abomasum or duodenum were 2.2-fold greater than those for after administration into the oral cavity (P < 0.05). The oral administration of 5 mg/kg BW of KP102 in the powder state, not dissolved in 9 ml of saline, failed to stimulate GH release. These results suggested that orally administered KP102 dissolved in saline transiently stimulates GH release in adult goats, and this phenomenon might be due to small amounts of the peptides entering directly into the abomasum with liquid bypassing the rumen.

Abomasum↗

Effects of magnetic fields on the accumulation of thiobarbituric acid reactive substances induced by iron salt and H(2)O(2) in mouse brain homogenates or phosphotidylcholine.

In this study, we examined the effects of magnetic fields (MFs) on the generation of thiobarbituric acid reactive substances (TBARS) in the mouse brain homogenates or phosphotidylcholine (PC) solution, incubated with FeCl(3) and/or H(2)O(2). Active oxygen species were generated and lipid peroxidation was induced in mouse brain homogenates by incubation with iron ions, resulting in the accumulation of TBARS. Lipid peroxidation was induced in PC by incubation with iron ions and H(2)O(2). Exposure to sinusoidal MFs (60 Hz, 0.2-1.2 mT), symmetric sawtooth-waveform MFs (50 Hz, 25-600 mT/s), rectangular MFs (1/0.4-1/16 Hz, 3.3 mT) and static MFs (1, 5-300 mT) had no effect on the accumulation of TBARS in brain homogenates induced by FeCl(3). In contrast, when the homogenates were incubated with FeCl(3) in static MFs (2-4 mT), the accumulation of TBARS was decreased. However, this inhibitory effect disappeared when EDTA was added to the homogenate and incubated with H(2)O(2). The accumulation of TBARS in PC solution incubated with FeCl(3) and H(2)O(2) was also inhibited by the static MF. These results indicate that only static MFs had an inhibitory effect on iron-induced lipid peroxidation and the effectiveness of this magnetic field on iron ion-induced active oxygen species generation is restricted to a so called 'window' of field intensity of 2-4 mT.

Journal Article↗

Characterization of four cell lines derived from a human malignant fibrous histiocytoma of the maxillary sinus.

We have established four cell lines from a human malignant fibrous histiocytoma. Each cell line had human aneuploid karyotype and DNA aneuploidy. Cells in all lines expressed CD13, CD68 and vimentin but lacked CD11, CD14, CD15, CD16, CD45, HLA class II and other mesenchymal and epithelial markers such as desmin, alpha-smooth muscle, myoglobin, S-100 protein, and cytokeratin. None of the cells expressed surface IgG or C3 receptor, nor did any of them phagocytose latex particles. The cells reacted with an antibody for prolyl-4-hydroxylase, but no collagen (types I, II, III, or IV) was detected in any of the cell lines. The homogenates of all cell lines had cyclic nucleotide phosphodiesterase 3 activity. Two cell lines produced granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-1alpha, IL-6 and tumor necrosis factor alpha, another line produced G-CSF, IL-1alpha, IL-6 and platelet-derived growth factor (PDGF)-AB, and the remaining cell line produced only PDGF-AB. None of the cells produced transforming growth factor-alpha. The results indicated that the cell lines were immunophenotypically similar to primitive mesenchymal cells.

3',5'-Cyclic-AMP Phosphodiesterases↗

Comparative linkage map development and identification of an autosomal locus for insensitive acetylcholinesterase-mediated insecticide resistance in Culex tritaeniorhynchus.

A comparative linkage map for Culex tritaeniorhynchus was constructed based on restriction fragment length polymorphism markers using cDNAs from Aedes aegypti. Linear orders of marker loci in Cx. tritaeniorhynchus were identical to Culex pipiens wherein chromosomes 2 and 3 reflect whole-arm rearrangements compared to A. aegypti. However, the sex determination locus in Cx. tritaeniorhynchus maps to chromosome 3, in contrast to Cx. pipiens and Ae. aegypti where it is located on chromosome 1. Our results indicate that insensitive acetylcholinesterase (AChE)-mediated organophosphate resistance is controlled by a single major gene (AChE) on chromosome 2, while the AChE structural gene (Ace) is located on chromosome 1. No evidence for a second Ace gene was observed, even under very low stringency hybridization conditions.

Acetylcholinesterase↗