Rhodium-catalyzed hydroarylation of alkynes with arylboronic acids: 1,4-shift of rhodium from 2-aryl-1-alkenylrhodium to 2-alkenylarylrhodium intermediate.
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Journal Article↗
Biomedical subjects
T Hayashi
Publications and source records attributed to T Hayashi.
A new stroke marker as detected by serum phosphoglycerate mutase B-type isozyme.
The diagnostic significance of phosphoglycerate mutase (PGM) B-type isozyme activity capable of being inducible under hypoxia at the gene level as a serum marker for cerebral stroke was investigated. The normal level (mean +/- 2 SD) in human serum was determined to be 38 +/- 18 units/L. Within 2 h after the onset of cerebral stroke (n = 65), B-type isozyme activity was elevated to 68 +/- 36 units/L, and retained to be higher level until 1-3 days. Serum B-type isozyme activities of 52 survival cases and 13 dead cases, being judged at the period of 1-2 months after the onset, were retrospectively compared; B-type isozyme activity that had been measured within 24 h after the onset was significantly higher (81 +/- 42 units/L) for the dead cases than for survival cases (57 +/- 27 units/L) with P < 0.05. These results suggest that serum PGM B-type isozyme has the potential as a novel marker for diagnosis of cerebral stroke and its severity.
Adolescent↗
Early decrease of redox factor-1 in spinal motor neurons of presymptomatic transgenic mice with a mutant SOD1 gene.
Oxidative stress has been proposed to play a pivotal role in pathogenesis of both sporadic and familial amyotrophic lateral sclerosis (ALS). Expression of DNA repair enzyme redox factor-1 (Ref-1) protein was examined in the spinal cord of transgenic mice with an ALS-linked mutant Cu/Zn superoxide dismutase (SOD1) gene. Immunoblotting and immunocytochemical analyses showed that the most spinal motor neurons lost the immunoreactivity for Ref-1 in the early presymptomatic stage that preceded significant loss of the neurons. The present result suggests that an early impairment of DNA repair in the spinal motor neurons may account for the mutant SOD1-mediated motor neuronal death in this model.
Amyotrophic Lateral Sclerosis↗
Differential antinociceptive effects induced by intrathecally administered endomorphin-1 and endomorphin-2 in the mouse.
Two highly selective mu-opioid receptor agonists, endomorphin-1 and endomorphin-2, have been identified and postulated to be endogenous ligands for mu-opioid receptors. Intrathecal (i.t.) administration of endomorphin-1 and endomorphin-2 at doses from 0.039 to 5 nmol dose-dependently produced antinociception with the paw-withdrawal test. The paw-withdrawal inhibition rapidly reached its peak at 1 min, rapidly declined and returned to the pre-injection levels in 20 min. The inhibition of the paw-withdrawal responses to endomorphin-1 and endomorphin-2 at a dose of 5 nmol observed at 1 and 5 min after injection was blocked by pretreatment with a non-selective opioid receptor antagonist naloxone (1 mg/kg, s.c.). The antinociceptive effect of endomorphin-2 was more sensitive to the mu (1)-opioid receptor antagonist, naloxonazine than that of endomorphin-1. The endomorphin-2-induced paw-withdrawal inhibition at both 1 and 5 min after injection was blocked by pretreatment with kappa-opioid receptor antagonist nor-binaltorphimine (10 mg/kg, s.c.) or the delta(2)-opioid receptor antagonist naltriben (0.6 mg/kg, s.c.) but not the delta(1)-opioid receptor antagonist 7-benzylidine naltrexone (BNTX) (0.6 mg/kg s.c.). In contrast, the paw-withdrawal inhibition induced by endomorphin-1 observed at both 1 and 5 min after injection was not blocked by naloxonazine (35 mg/kg, s.c.), nor-binaltorphimine (10 mg/kg, s.c.), naltriben (0.6 mg/kg, s.c.) or BNTX (0.6 mg/kg s.c.). The endomorphin-2-induced paw-withdrawal inhibition was blocked by the pretreatment with an antiserum against dynorphin A-(1-17) or [Met(5)]enkephalin, but not by antiserum against dynorphin B-(1-13). Pretreatment with these antisera did not affect the endomorphin-1-induced paw-withdrawal inhibition. Our results indicate that endomorphin-2 given i.t. produces its antinociceptive effects via the stimulation of mu (1)-opioid receptors (naloxonazine-sensitive site) in the spinal cord. The antinociception induced by endomophin-2 contains additional components, which are mediated by the release of dynorphin A-(1-17) and [Met(5)]enkephalin which subsequently act on kappa-opioid receptors and delta(2)-opioid receptors to produce antinociception.
Analgesics↗
The superiority of organically cultivated vegetables to general ones regarding antimutagenic activities.
We found organically cultivated (OC) vegetables, using a water-soluble chitosan as a soil improvement agent and leaf surface spray, had much longer shelf life and better taste than that of generally cultivated (GC) vegetables. The purpose of this study is to determine the relative antimutagenic activity between OC and GC vegetables. Eleven OC vegetables were harvested in March and April in 1999 and 2000, and GC ones were supplied as a control from nearby farms on the same date. The former vegetables were planted on the field where no pesticide had been used for the last 3 years. Forward mutation test with Salmonella typhimurium TM677 and 8-azaguanine as a detection agent was used to determine the antimutagenic activity of juices prepared from OC and GC vegetables against authentic mutagens, such as 4-nitroquinoline oxide (4NQO), benzo(a)pyrene (BaP), and 3-amino-1-methyl-5H-pyrido[4,3-b]indole acetate (Trp-P-2). This microbiological test is a convenient method to use for the food samples containing free histidine. Antimutagenic activity was evaluated by the difference of mutagenic activities between mutagenecity of authentic compounds and that observed upon incubation at 37 degrees C for 2h with each vegetable juice. OC Chinese cabbage, carrot, Welsh onion, and Qing-gen-cai suppressed 37-93% of the mutagenic activity of 4NQO, while the GC ones were held down to 11-65%. Against BaP, three species of OC vegetables showed 30-57% antimutagenecity, while GC ones did only 5-30%. Similarly, the OC spinach decreased the activity of Trp-P-2 to 78%, and the GC suppressed it by 49%.
Animals↗
Treatment outcome of maxillary sinus squamous cell carcinoma.
BACKGROUND: Optimal treatment policies of maxillary sinus carcinoma remain to be defined. METHODS: Seventy-four patients with squamous cell carcinoma of maxillary sinus were treated at Department of Otolaryngology, Asahikawa Medical College between 1983 and 1997. The T classification according to the 1997 International Union Against Cancer was as follows: 9 with T2, 35 with T3, and 30 with T4. Eight patients had lymph node metastasis with N1 at diagnosis. Of 62 patients who started multimodality therapy that comprised preoperative radiochemotherapy including local irradiation with total dose of 50 grays along with concomitant intramaxillary arterial infusion of 5-fluorouracil with total dose of 5000 mg followed by total or partial maxillectomy, 59 received the complete therapy. Eleven patients had to be treated with radiotherapy alone, and 1 patient received postoperative radiotherapy. The median follow-up time for surviving patients was 117 months. RESULTS: The 5-year overall survival, disease free survival, and local control (LC) rates for all patients were 58.5%, 63.7%, and 73.6%, respectively. The patients who underwent multimodality therapy showed significantly better 5-year overall survival, disease free survival, and LC rates as compared with those who underwent radiotherapy alone (68.5% vs. 9.1%; 73.2% vs. 18.2%; 84.0% vs. 18.2%; P < 0.0001 each). Multivariate analysis revealed that T classification and treatment modality are independent predictors for disease free survival. CONCLUSIONS: The authors' treatment method, which did not include any complicated techniques, produced higher survival and LC rates because of high effectiveness of multimodality therapy. They concluded that their multimodality therapy could offer a better chance for cure from maxillary sinus carcinoma at many institutions.
Carcinoma, Squamous Cell↗
Expressions of nitrotyrosine and TUNEL immunoreactivities in cultured rat spinal cord neurons after exposure to glutamate, nitric oxide, or peroxynitrite.
Although excitotoxic and oxidative stress play important roles in spinal neuron death, the exact mechanism is not fully understood. We examined cell damage of primary culture of 11-day-old rat spinal cord by addition of glutamate, nitric oxide (NO) or peroxynitrite (PN) with detection of nitrotyrosine (NT) or terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL). With addition of glutamate, NOC18 (a slow NO releaser) or PN, immunoreactivity for NT became stronger in the cytoplasm of large motor neurons in the ventral horn at 6 to 48 hr and positive in the axons of the ventral horn at 24 to 48 hr. TUNEL positive nuclei were found in spinal large motor neurons from 24 hr, and the positive cell number greatly increased at 48 hr in contrast to the vehicle. Pretreatment of cultures with alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor antagonist, NO-suppressing agent, and antioxidant protected the immunoreactivity for NT or TUNEL. The present results suggest that both excitotoxic and oxidative stress play an important role in the upregulation of NT nitration and the apoptotic pathway in cultured rat spinal neurons.
Animals↗
Estrogen prevents destabilization of endothelial nitric oxide synthase mRNA induced by tumor necrosis factor alpha through estrogen receptor mediated system.
17beta-estradiol up-regulates endothelial nitric oxide synthase (eNOS) expression in cultured endothelial cells. To clarify the role of mRNA stabilization in upregulation of eNOS expression, endothelial cells were incubated with actinomycin D as transcriptional inhibitor. Up to 10 hours incubation with 17beta-estradiol alone did not affect significantly the stability of eNOS mRNA. As tumor necrosis factor-alpha (TNF-alpha) is associated with the progression of atherosclerosis, we examined the effect of 17beta-estradiol on eNOS mRNA destabilization with TNF-alpha. After 10 hours co-incubation with TNF-alpha, relative intensity of eNOS mRNA decreased to 50% of the intensity at the start time of incubation, however, it remained significantly 1.6 times in the presence of 17beta-estradiol. This inhibitory effect of 17beta-estradiol was abolished by the treatment of estrogen receptor antagonist, ICI 182,780. This is the first finding that 17beta-estradiol stabilizes eNOS mRNA destabilized by TNF-alpha through estrogen receptor mediated mechanism.
Animals↗
A novel SOD1 gene mutation in familial ALS with low penetrance in females.
We identified a novel missense mutation in the Cu/Zn superoxide dismutase gene in a family with amyotrophic lateral sclerosis (ALS). The mutation was a transition of T to C, resulting in a substitution of leucine 126 to serine in exon 5. The family had very unique clinical features of extremely mild severity only in the legs of two male patients with onset of 42 and 52 years old, and their mothers did not develop any symptom even after reaching the age of 80 and carrying the same mutation. The present study suggests that there are other factors that delay or prevent the disease.
Adult↗
Impaired retrograde axonal transport of adenovirus-mediated E. coli LacZ gene in the mice carrying mutant SOD1 gene.
A replication-defective recombinant adenoviral vector containing E. coli lacZ gene was injected into the gastrocnemius muscles of transgenic mice carrying mutant Cu/Zn superoxide dismutase (SOD1) gene and non-transgenic wild-type mice at 40 weeks of age. After 60 and 90 h of the injection, lacZ staining was observed at the distal ends of the sciatic nerves in both mice groups, with the number and the distances greatly reduced in the transgenic mice. Mean velocities of retrograde transport for lacZ was estimated to be 2.1 and 0.05 mm/24 h in non-transgenic and transgenic mice, respectively. These results indicate that the retrograde axonal transport of foreign gene product is impaired in the mice model for familial amyotrophic lateral sclerosis.
Adenoviridae↗
[Hemophagocytic syndrome].
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Collagen Diseases↗
Chloroprene as a source of fine chemicals: palladium-catalyzed synthesis of terminal allenes.
[reaction: see text] Several functionalized terminal allenes were prepared in moderate to excellent yield by a palladium-catalyzed reaction of chloroprene (2-chloro-1,3-butadiene) with soft nucleophiles.
Journal Article↗
Immunostimulatory DNA-based vaccines elicit multifaceted immune responses against HIV at systemic and mucosal sites.
Immunostimulatory DNA sequences (ISS, also known as CpG motifs) are pathogen-associated molecular patterns that are potent stimulators of innate immunity. We tested the ability of ISS to act as an immunostimulatory pathogen-associated molecular pattern in a model HIV vaccine using gp120 envelope protein as the Ag. Mice immunized with gp120 and ISS, or a gp120:ISS conjugate, developed gp120-specific immune responses which included: 1) Ab production; 2) a Th1-biased cytokine response; 3) the secretion of beta-chemokines, which are known to inhibit the use of the CCR5 coreceptor by HIV; 4) CTL activity; 5) mucosal immune responses; and 6) CD8 T cell responses that were independent of CD4 T cell help. Based on these results, ISS-based immunization holds promise for the development of an effective preventive and therapeutic HIV vaccine.
AIDS Vaccines↗
Cerivastatin, a hydroxymethylglutaryl coenzyme a reductase inhibitor, improves endothelial function in elderly diabetic patients within 3 days.
BACKGROUND: The short-term effects of hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) on endothelial function at doses that do not affect plasma lipid levels are not known. METHODS AND RESULTS: We investigated the short-term effects of cerivastatin, a hydroxymethylglutaryl coenzyme A reductase inhibitor, on endothelial function and endothelium-related products in elderly diabetic patients. Twenty-seven elderly diabetic patients (aged 69.3+/-3.4 years), with or without mild hypercholesterolemia, were enrolled in this study, which tested cerivastatin treatment (0.15 mg/d) for 3 days. Endothelium-dependent flow-mediated dilatation, endothelium-independent dilatation by nitroglycerin in the brachial artery, nitric oxide-related products (nitrite/nitrate and cGMP), endothelium-related products (von Willebrand Factor, soluble vascular cell adhesion molecule-1, and soluble intercellular adhesion molecule-1), and a marker of oxidant stress (8-isoprostane) were assessed. Levels of plasma lipids were not changed before and after treatment with cerivastatin. Flow-mediated dilatation was significantly increased by cerivastatin treatment, as were plasma nitrite/nitrate levels (from 16.9+/-3.4 to 22.0+/-3.7 micromol/L, P<0.05) and cGMP values. The percent of nitroglycerin-induced dilatation was not changed. Plasma concentrations of 8-isoprostane decreased, and levels of soluble vascular cell adhesion molecule also tended to decrease with cerivastatin. CONCLUSIONS: Improvement of endothelial function was in line with antiatherosclerotic effects. Cerivastatin improved impaired endothelial function in the short-term without affecting lipid profiles in elderly diabetic patients. This effect may be partly due to upregulation of endothelial nitric oxide synthase.
Aged↗
Expression of polysialylated neural cell adhesion molecule in rat brain after transient middle cerebral artery occlusion.
The highly polysialylated form of neural cell adhesion molecule (PSA-NCAM) is important for neurite outgrowth. With this molecule as a marker of plastic change in neurons, we investigated its temporal expression in rat brain after transient middle cerebral artery (MCA) occlusion. In sham-control brain, only subependymal neurons showed a positive immunoreactivity for PSA-NCAM. After 90 min of transient MCA occlusion, neurons in the piriform cortex began to be positively stained at 1 h, while neurons in the cortex and caudate of the MCA territory became positive after 8 h. The stainings persisted for 1 and 3 days after reperfusion. The present results indicate that neurons in the cerebral cortex and caudate have the capability of plastic change in the adult brain, and that those in the piriform cortex rapidly undergo plastic change probably in response to transneuronal injury.
Animals↗
First confirmed canine case of Ehrlichia canis infection in Japan.
An 11-year-old castrated Pekinese dog that had been moved from Indonesia to Japan eight years previously was diagnosed with an Ehrlichia canis infection by haematological characteristics (normocytic anaemia, mild thrombocytopenia and hypergammaglobulinaemia) and serological findings (antibody titre to E canis 1:3,200 or more). The dog did not respond to treatment with tetracycline and died from renal failure. The diagnosis was confirmed postmortem by pathological evaluation and polymerase chain reaction (PCR) followed by sequencing of the 16S rRNA gene. Typical morulae of Ehrlichia were detected in the cytoplasm of macrophages in spleen tissue by immunohistological staining. Ehrlichia-like organisms were also detected in the spleen by electron microscopy. E canis-specific PCR analysis of DNA extracted from the spleen gave a positive signal, and sequence analysis of the fragment revealed that it was identical to part of the 16s rRNA gene of E canis. The dog was the first confirmed clinical case of E canis infection in Japan.
Animals↗
Time dependent amelioration against ischemic brain damage by glial cell line-derived neurotrophic factor after transient middle cerebral artery occlusion in rat.
Time dependent influence of glial cell line-derived neurotrophic factor (GDNF) was examined after 90 min of transient middle cerebral artery occlusion (MCAO) in rats. Treatment with GDNF significantly reduced the infarct volume stained with 2,3,5-triphenyltetrazolium chloride (TTC) when GDNF was topically applied at 0 and 1 h of reperfusion, but became insignificant at 3 h as compared to vehicle group. The protective effect of GDNF was closely related to the significant reduction of the number of terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) positive cells as well as immunofluorescently positive cells for active forms of caspases, especially active caspase-3 but not -9. Thus, the present study showed that topical application of GDNF significantly reduced infarct size in a time-dependent manner, while the therapeutic time window was shorter than other chemical compounds such as an NMDA receptor antagonist (MK-801) and a free radical scavenger (alpha-phenyl-tert-butyl-nitrone, PBN). The effect of GDNF was stronger in suppressing active caspase-3 than active caspase-9.
Animals↗
Induction of highly polysialylated neural cell adhesion molecule (PSA-NCAM) in postischemic gerbil hippocampus mainly dissociated with neural stem cell proliferation.
We investigated a possible expression of highly polysialylated neural cell adhesion molecule (PSA-NCAM) in gerbil hippocampus after 5 min of transient global ischemia in association to the proliferation of neural stem cell labeled with bromodeoxyuridine (BrdU). The number of PSA-NCAM positive cells increased in the granule cell layer (GCL) of dentate gyrus (DG) by 1.9 to 2.7-fold at 10 and 20 days after the reperfusion. The number of BrdU-labeled cells increased mainly in the subgranular zone of DG by 7.2 to 8.0-fold at 5 and 10 days after the reperfusion. Immunofluorescence for PSA-NCAM and BrdU showed that the majority of DG cells were not double labeled, while one or two cells per section were double labeled in the deepest portion of the GCL only at 10 days after the reperfusion. These results suggest different predominant spatial distribution and chronological change of PSA-NCAM positive and BrdU-labeled cells in DG after transient ischemia.
Animals↗