English phonology and an acoustic language universal.

Acoustic analyses of eight different languages/dialects had revealed a language universal: Three spectral factors consistently appeared in analyses of power fluctuations of spoken sentences divided by critical-band filters into narrow frequency bands. Examining linguistic implications of these factors seems important to understand how speech sounds carry linguistic information. Here we show the three general categories of the English phonemes, i.

Rat white adipocytes activate p85/p110 PI3K and induce PM GLUT4 in response to adrenoceptor agonists or aluminum fluoride.

Adipocyte responses to adrenergic and ß-adrenoceptor(-AR) (adrenoceptor) regulation are not sufficiently understood, and information helpful for elucidating the adrenoceptor-responsive machinery is insufficient. Here we show by using immunoprecipitated kinase analysis with a phosphatidylinositol 3-kinase (PI3K) p85 antibody that PI3K activation was induced by treatment with 10 or 100 µM norepinephrine (NE) for 15 min or with 10 mM aluminum fluoride (AF, a guanosine triphosphate (GTP)-binding (G) protein activator) for 20 min in white adipocytes (rat epididymal adipocytes) and that treatment with pertussis toxin (PTX, a G-protein inactivator) inhibited PI3K activation induced by the 20-min treatment with AF in the cells. In addition, western blot analysis revealed that glucose transporter 4 (GLUT4) level in the adipocyte plasma membrane (PM) fraction was increased by treatment with 10 µM NE, 100 µM dobutamine (DOB, a ß1-AR agonist), or 0.

CL316243 induces phosphatidylinositol 3,4,5-triphosphate production in rat adipocytes in an adenosine deaminase-, pertussis toxin-, or wortmannin-sensitive manner.

The effect of beta(3)-adrenoceptor (beta(3)-AR) agonists on adipocytes treated or not treated with signaling modulators has not been sufficiently elucidated. Using rat epididymal adipocytes (adipocytes) labeled with [(32)P]orthophosphate, we found that treatment with the selective beta(3)-AR agonist CL316243 (CL; 1 microM) induces phosphatidylinositol (PI) 3,4,5-triphosphate (PI[3,4,5]P(3)) production and that this response is inhibited by adenosine deaminase (ADA, an adenosine-degrading enzyme; 2 U/ml), pertussis toxin (PTX, an inactivator of inhibitory guanine-nucleotide-binding protein; 1 microg/ml), or wortmannin (WT, a PI-kinase inhibitor; 3 microM). The results showed that CL induced PI(3,4,5)P(3) production in intact adipocytes and that this production was affected by signaling modulators.

Adipose cells induce phospho-Thr-172 AMPK production by epinephrine or CL316243 in mouse 3T3-L1 adipocytes or MAPK activation and G protein-associated PI3K responses induced by CL316243 or aluminum fluoride in rat white adipocytes.

Responses of adipose cells to adrenoceptor regulation, including that of β-adrenoceptor (AR), and the signalling machinery involved in these responses are not sufficiently understood; information that is helpful for elucidating the adrenoceptor (adrenergic and β-AR)-responsive machinery is insufficient. We examined phospho-Thr-172 AMPK production in mouse-derived 3T3-L1 adipocytes treated with epinephrine or CL316243 (a β3-AR agonist) for 15 min. We also examined MAPK activation or G protein-associated PI3K activation or -associated PI3K p85 complex formation in rat epididymal (white) adipocytes treated with CL316243 for 15 min or aluminum fluoride (a G-protein signalling activator) for 20 min.

3T3-L1 adipocytes possess anandamide- and epinephrine-responsive machinery for MDM2 distribution to the plasma membrane.

The effects of biomolecules on peripheral tissues and their responsive machinery are not well understood. We examined MDM2 level in the plasma membrane (PM) and total MDM2 level of 3T3-L1 adipocytes treated with biomolecular anandamide, epinephrine, and other agents for 15 min. We also examined biomolecular responses in cells treated with mithramycin A, a binding inhibitor, or cells exposed to cooling and cell viability.

Polymorphisms in the 5'-UTR of PTEN and other gene polymorphisms in normal Japanese individuals.

Polymorphisms are distributed differently in populations, including those of regions, ethnic groups, and diseased patients. In order to investigate variation in nucleotide sequences in normal individuals, we isolated genomic DNA from the blood of healthy Japanese individuals and sequenced the 5'-untranslated region (5'-UTR) of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene and the gene promoter, intron, and exon nucleotides of p53, p14(ARF), murine double minute 2 (MDM2), and the beta2- and beta3-adrenoceptor (-AR). We found polymorphisms in these regions, including a deletion at positions -465 to -463 and a substitution at position -404 in PTEN and a substitution at position -4924 in p14(ARF), in normal individuals.

Cooling-increased phospho-β-arrestin-1 and β-arrestin-1 expression levels in 3T3-L1 adipocytes.

Cooling induces several responses that are modulated by molecular inhibitors and activators and receptor signaling. Information regarding potential targets involved in cold response mechanisms is still insufficient. We examined levels of the receptor-signaling mediator β-arrestin-1 and phospho-Ser-412 β-arrestin-1 in 3T3-L1 adipocytes exposed to 4-37 °C or treated with some molecular agents at 37°C.

Polymorphisms in promoter sequences of MDM2, p53, and p16 genes in normal Japanese individuals.

Research has been conducted to identify sequence polymorphisms of gene promoter regions in patients and control subjects, including normal individuals, and to determine the influence of these polymorphisms on transcriptional regulation in cells that express wild-type or mutant p53. In this study we isolated genomic DNA from whole blood of healthy Japanese individuals and sequenced the promoter regions of the MDM2, p53, and p16(INK4a) genes. We identified polymorphisms comprising 3 nucleotide substitutions at exon 1 and intron 1 regions of the MDM2 gene and 1 nucleotide insertion at a poly(C) nucleotide position in the p53 gene.

MDM2-related responses in 3T3-L1 adipocytes exposed to cooling and subsequent rewarming.

Insulin-like growth factor-I and insulin induce the production of phospho-Ser-166 MDM2, a target of Akt, and influence the formation of the MDM2 complex. The glycolipid hormone insulin differentially activates phosphatidylinositol 3-kinase (PI3K)/Akt pathways in 3T3-L1 (L1) adipocytes incubated at 19 °C. Responses of L1 adipocytes to different temperature changes and their regulatory mechanisms are poorly understood.

Induction of phospho-Thr-172 AMPK in 3T3-L1 adipocytes exposed to cold or treated with anisomycin, mithramycin A, and ionic compounds.

Cold exposure induces cellular responses, including subcellular molecule expression and transport responses, similar to those stimulated by insulin in 3T3-L1 (L1) adipocytes. The transport response is induced in L1 adipocytes treated with translation inhibitors. We examined the level of phospho-Thr-172 AMPK (an active form of AMPK, a known energy-state sensor) in L1 adipocytes exposed to different temperatures of 4-37 degrees C or stressors, including chemical inhibitors and activators.

Polymorphisms in promoter sequences of the p15 ( INK4B ) and PTEN genes of normal Japanese individuals.

Gene promoter regions of p15(INK4B), a cyclin-dependent kinase inhibitor, and phosphatase and tensin homolog (PTEN), a dual-function protein and lipid phosphatase, interact with regulatory factors for gene transcription and methylation. Normal individuals exhibit sequence polymorphisms in these regulatory genes. We isolated genomic DNA from whole blood of healthy Japanese individuals and sequenced promoter regions of the p15 ( INK4B ) and PTEN genes.

Chloroform deposition in renal cyst fluid of hemodialysis patients with renal cystic disorders.

Chronic exposure to chloroform (CHCl3) induces renal neoplasms in rodents and may be carcinogenic in humans, but studies on chronic CHCl3 deposition in the human body have not been performed. In this study, we examined 27 hemodialysis patients with renal cystic diseases including acquired cystic disease of the kidney (ACDK) accompanied by renal tumors at high frequency. Intracystic and serum CHCl3 concentrations were determined using a headspace gas chromatography/mass spectrometry analysis.

Cancer prevention by phytochemicals.

Information has been accumulated indicating that diets rich in vegetables and fruits can reduce the risk of a number of chronic diseases, including cancer, cardiovascular disease, diabetes and age-related macular degeneration. Phytochemicals (various factors in plant foods), such as carotenoids, antioxidative vitamins, phenolic compounds, terpenoids, steroids, indoles and fibers, have been considered responsible for the risk reduction. Among them, a mixture of natural carotenoids has been studied extensively and proven to show beneficial effects on human cancer prevention.

Carotenoids in cancer chemoprevention.

Various natural carotenoids, besides beta-carotene, were proven to have anticarcinogenic activity, and some of them showed more potent activity than beta-carotene. Thus, these carotenoids (alpha-carotene, lutein, zeaxanthin, lycopene, beta-cryptoxanthin, fucoxanthin, astaxanthin, capsanthin, crocetin and phytoene), as well as beta-carotene, may be useful for cancer prevention. In the case of phytoene, the concept of 'bio-chemoprevention', which means biotechnology-assisted method for cancerchemoprevention, may be applicable.

Epinephrine does not reduce the plasma concentration of lidocaine during continuous epidural infusion in children.

Purpose: During continuous epidural anesthesia with lidocaine, plasma monoethylglycinexylidide (MEGX), an active metabolite of lidocaine, increases continuously. We assessed the effect of epinephrine on the absorption of lidocaine and the accumulation of MEGX during continuous epidural anesthesia in children.

Methods: Anesthesia was administered as an initial bolus of 5 mg x kg(-1) of 1% lidocaine solution followed by continuous infusion at 2.

Phosphorylation of c-Jun N-terminal kinase in human hepatoblastoma cells is transiently increased by cold exposure and further enhanced by subsequent warm incubation of the cells.

During a cold preservation and reperfusion process of organs, cells are exposed to two major stresses, i.e. changes in oxygen concentration and temperature.

Cold-stimulated increase in a regulatory subunit of cAMP-dependent protein kinase in human hepatoblastoma cells.

Although cold-stress responses in bacteria and plants have been well studied and hypothermic conditions are used in clinical treatments, there has been little investigation of cold-stress responses in human cells, and there has been no report on the involvement of signal transduction modulators in the cold-stress response in human cells. We therefore investigated alterations in the expression of genes involved in the signal transduction system and the mechanisms of cold-stimulated increases in the expression of genes in human hepatoblastoma (HepG2) cells. Using a cDNA expression array method, we found that a transcript encoding a regulatory subunit Ibeta (RIbeta) of cyclic AMP-dependent protein kinase (PKA) was increased in cold-stressed cells.

[Prediction of the need for mechanical ventilation after transsternal thymectomy in patients with myasthenia gravis].

Between June 1992 and May 2000, transsternal extended thymectomy was performed for 70 patients with myasthenia gravis in our hospital. We were able to evaluate 64 of them in terms of prediction of the need for postoperative mechanical ventilation using the score systems reported by Leventhal et al., Kimura et al.

[The analysis of surgically treated pulmonary tuberculosis].

Between January 1990 and December 1999, thirteen patients with pulmonary tuberculosis underwent surgical management in our hospital. The purpose of surgery was classified into three groups: drug-resistant or persistent disease (7 patients), hemoptysis (3), and the others. We have no operative death, but have two late deaths due to postoperative persistent positive sputum and progressive tuberculosis infection.

Mitochondrial genome-encoded ATPase subunit 6+8 mRNA increases in human hepatoblastoma cells in response to nonfatal cold stress.

Cellular responses to cold stress have not been well clarified, compared with heat shock responses, especially in mammalian cells. We investigated cold-stress responses in human hepatoblastoma cells (HepG2) exposed to a nonfatal temperature of 17 degrees C. Under the condition, RNA and protein syntheses in the cells were highly, but incompletely, depressed and cell growth was impaired.

[Postoperative interstitial pneumonia: 2 cases after lobectomy].

Two patients with postoperative interstitial pneumonia are reported. Preoperative diagnosis was primary lung cancer without idiopathic interstitial pneumonia (IIP). Within one week after operation acute interstitial pneumonia (AIP) occurred on the nonoperated side and developed.

[Surgical management of pulmonary disease due to nontuberculous mycobacteria].

Between 1983 and 1998, 9 patients with nontuberculous mycobacteriosis (NTM) underwent pulmonary resection. 8 patients were men and 1 was woman. Mean length of preoperative period was 20.

Comparison of atypical beta3-adrenoceptor agonists with their respective metabolic activities in rat white adipocytes.

The metabolic activities of four types of beta3-adrenoceptor (AR) agonists, BRL35135A, BRL28410, ICI215001 and CL316243, were compared with those of other beta1- and beta2-AR agonists in rat white adipocytes. All the beta3-AR agonists caused cAMP formation, free fatty acid release and 2-deoxyglucose uptake; the maximum activity levels were similar except for ICI215001, which was lower. However, the magnitude of potency and selectivity of these agonists differed.

Suppression of insulin-stimulated phosphatidylinositol 3-kinase activity by the beta3-adrenoceptor agonist CL316243 in rat adipocytes.

Insulin increased 2-deoxyglucose (2-DG) uptake via the translocation of glucose transporter (GLUT) 4 to the plasma membrane fraction in rat adipocytes. The stimulatory actions of insulin were accompanied by both an increase in the immunoreactive p85 subunit of phosphatidylinositol (PI) 3-kinase in the plasma membrane fractions and PI 3-kinase activation by tyrosine phosphorylation of the p85 subunit. The beta3-adrenoceptor agonist CL316243 (CL) suppressed all the insulin actions in adenosine deaminase (ADA)-treated cells, but was without effect in non-ADA-treated cells.

Immunological study of unresponsive state in rat hepatic transplant model. 2. Immunosuppressive factor in the serum from the tolerant hosts.

Our previous study demonstrated that Lewis (LEW) rat recipients engrafted with Brown-Norway (BN) rat liver displayed a long-term graft survival and that phenotypic and functional analyses of graft-infiltrating cells on day 6 postgrafting showed a lower proportion and activity of cytotoxic cells in long-term surviving hosts than LEW recipients engrafted with DA rat liver which showed acute rejection on day 9 postgrafting. In order to assess the immunological mechanisms of unresponsiveness, we analyzed the lymphocyte and serum from LEW recipients engrafted with BN liver. Spleen cells from tolerant LEW recipients on day 6 posttransplantation had no suppressor effect on the one-way mixed lymphocyte culture (MLC) reaction.