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K Fukuda

Publications and source records attributed to K Fukuda.

At least 145 records · Page 8Linked to original sources

Inhibition of the human intermediate conductance Ca(2+)-activated K(+) channel, hIK1, by volatile anesthetics.

Ca(2+)-activated K(+) channels (K(Ca)) regulate a wide variety of cellular functions by coupling intracellular Ca(2+) concentration to membrane potential. There are three major groups of K(Ca) classified by their unit conductances: large (BK), intermediate (IK), and small (SK) conductance of channels. BK channel is gated by combined influences of Ca(2+) and voltage, while IK and SK channels are gated solely by Ca(2+). Volatile anesthetics inhibit BK channel activity by interfering with the Ca(2+) gating mechanism. However, the effects of anesthetics on IK and SK channels are unknown. Using cloned IK and SK channels, hIK1 and hSK1-3, respectively, we found that the currents of hIK1 were inhibited rapidly and reversibly by volatile anesthetics, whereas those of SK channels were not affected. The IC(50) values of the volatile anesthetics, halothane, sevoflurane, enflurane, and isoflurane for hIK1 inhibition were 0.69, 0.42, 1.01 and 1.03 mM, respectively, and were in the clinically used concentration range. In contrast to BK channel, halothane inhibition of hIK1 currents was independent of Ca(2+) concentration, suggesting that Ca(2+) gating mechanism is not involved. These results demonstrate that volatile anesthetics, such as halothane, enflurane, isoflurane, and sevoflurane, affect BK, IK, and SK channels in distinct ways.

Anesthetics, Inhalation↗

Surveillance for influenza--United States, 1994-95, 1995-96, and 1996-97 seasons.

PROBLEM/CONDITION: Influenza epidemics occur nearly every year during the winter months and are responsible for substantial morbidity and mortality in the United States, including an average of approximately 114,000 hospitalizations and 20,000 deaths per year. REPORTING PERIOD: This report summarizes U.S. influenza surveillance data from October 1994 through May 1997, from both active and passive surveillance systems. DESCRIPTION OF SYSTEM: During the period covered, CDC received weekly reports from October through May from a) state and territorial epidemiologists on estimates of local influenza activity, b) approximately 140 sentinel physicians on their total number of patient visits and the number of cases of influenza-like illness (ILI), and c) approximately 70 World Health Organization (WHO) collaborating laboratories in the United States on weekly influenza virus isolations. WHO collaborating laboratories also submitted influenza isolates to CDC for antigenic analysis. Throughout the year, vital statistics offices in 121 cities reported deaths related to pneumonia and influenza (P&I) weekly, providing a measure of the impact of influenza on mortality. RESULTS: During the 1994-95 influenza season, 25 state epidemiologists reported regional or widespread activity at the peak of the season. Cases of ILI reported by sentinel physicians exceeded baseline levels for 4 weeks, peaking at 5%. Influenza A(H3N2) was the most frequently isolated influenza virus type/subtype. The longest period of sustained excess mortality was 5 consecutive weeks, when the percentage of deaths attributed to P&I exceeded the epidemic threshold, peaking at 7.6%. During the 1995-96 season, 33 state epidemiologists reported regional or widespread activity at the peak of the season. ILI cases exceeded baseline levels for 5 weeks, peaking at 7%. Influenza A(H1N1) viruses predominated, although influenza A(H3N2) and influenza B viruses also were identified throughout the United States. P&I mortality exceeded the epidemic threshold for 6 consecutive weeks, peaking at 8.2%. The 1996-97 season was the most severe of the three seasons summarized in this report. Thirty-nine state epidemiologists reported regional or widespread activity at the peak of the season. ILI reports exceeded baseline levels for 5 consecutive weeks, peaking at 7%. The proportion of respiratory specimens positive for influenza peaked at 34%, with influenza A(H3N2) viruses predominating. Influenza B viruses were identified throughout the United States, but only one influenza A(H1N1) virus isolate was reported overall. The proportion of deaths attributed to P&I exceeded the epidemic threshold for 10 consecutive weeks, peaking at 9.1%. INTERPRETATION: Influenza A(H1N1), A(H3N2), and B viruses circulated during 1994-1997. Local surveillance data are important because of geographic and temporal differences in the circulation of influenza types/subtypes. PUBLIC HEALTH ACTIONS: CDC conducts active national surveillance annually from October through May for influenza to detect the emergence and spread of influenza virus variants and monitor the impact of influenza-related morbidity and mortality. Surveillance data are provided weekly throughout the influenza season to public health officials, WHO, and health-care providers and can be used to guide prevention and control activities, vaccine strain selection, and patient care.

Humans↗

Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP).

This report updates 1999 recommendations by the Advisory Committee on Immunization Practices (ACIP) on the use of influenza vaccine and antiviral agents (MMWR 1999;48[No. RR-4]: 1-29). These recommendations include five principal changes: a) the age for universal vaccination has been lowered to 50 years from 65 years; b) scheduling of large, organized vaccination campaigns after mid-October may be considered because the availability of vaccine in any location cannot be assured consistently in the early fall; c) 2000-2001 trivalent vaccine virus strains are A/Moscow/10/99 (H3N2)-like, A/New Caledonia/20/99 (H1N1)-like, and B/Beijing/184/93-like strains; d) information on neuraminidase-inhibitor antiviral drugs has been added; and e) a list of other influenza-related infection control documents for special populations has been added. This report and other information on influenza can be accessed at the website for the Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC at .

Adolescent↗

Autocrine/Paracrine secretion of IL-6 family cytokines causes angiotensin II-induced delayed STAT3 activation.

We recently reported that angiotensin II (AngII) biphasically activates the JAK/STAT pathway and induces delayed phosphorylation of STAT3 in the late stage (120 min) in cardiomyocytes. This study was designed to determine the mechanism of delayed phosphorylation of STAT3. Conditioned medium prepared from AngII-stimulated cardiomyocytes could reproduce the tyrosine phosphorylation of STAT3 at 5 min. This delayed phosphorylation was almost completely inhibited by anti-gp130 blocking antibody RX435, but not by TAK044 (ET-A/B-R antagonist), prazosin, or propranolol. AngII induced phosphorylation of gp130 in the late stage, which was temporally in parallel with the delayed phosphorylation of STAT3. AngII augmented IL-6, CT-1, and LIF mRNA expression at 30-60 min, but not CNTF expression. AngII increased IL-6 protein levels by 3-fold in the conditioned media at 2 h compared with the control. These findings indicated that AngII-induced delayed activation of STAT3 is caused by autocrine/paracrine secreted IL-6 family cytokines.

Angiotensin II↗

Effects of 6-formylpterin, a xanthine oxidase inhibitor and a superoxide scavenger, on production of nitric oxide in RAW 264.7 macrophages.

As well as superoxide generated from neutrophils, nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) in macrophages plays an important role in inflammation. We previously showed that 6-formylpterin, a xanthine oxidase inhibitor, has a superoxide scavenging activity. In the present study, to elucidate other pharmacological activities of 6-formylpterin, we investigated the effects of 6-formylpterin on production of nitric oxide (NO) in the murine macrophage cell line RAW 264.7 stimulated by lipopolysaccharide (LPS) and interferon-gamma (INF-gamma). 6-Formylpterin suppressed the expression of iNOS, and it also inhibited the catalytic activity of iNOS, which collectively resulted in the inhibition of NO production in the stimulated macrophages. However, 6-formylpterin did not scavenge the released NO from an NO donor, S-nitroso-N-acetylpenicillamine (SNAP). These results indicate that 6-formylpterin inhibits pathological NO generation from macrophages during inflammation, but that it does not disturb the physiological action of NO released from other sources.

Animals↗

Crystal structure of flavocetin-A, a platelet glycoprotein Ib-binding protein, reveals a novel cyclic tetramer of C-type lectin-like heterodimers.

Snake venom contains a number of the hemostatically active C-type lectin-like proteins, which affect the interaction between von Willebrand factor (vWF) and the platelet glycoprotein (GP) Ib or platelet receptor to inhibit/induce platelet activation. Flavocetin-A (FL-A) is a high-molecular mass C-type lectin-like protein (149 kDa) isolated from the habu snake venom. FL-A binds with high affinity to the platelet GP Ibalpha-subunit and functions as a strong inhibitor of vWF-dependent platelet aggregation. We have determined the X-ray crystal structure of FL-A and refined to 2.5 A resolution. This is a first elucidation of a three-dimensional structure of the platelet GP Ib-binding protein. The overall structure reveals that the molecule is a novel cyclic tetramer (alphabeta)(4) made up of four alphabeta-heterodimers related by a crystallographic 4-fold symmetry. The tetramerization is mediated by an interchain disulfide bridge between cysteine residues at the C-terminus of the alpha-subunit and at the N-terminus of the beta-subunit in the neighboring alphabeta-heterodimer. The high affinity of FL-A for the platelet GP Ib alpha-subunit could be explained by a cooperative-binding action through the multiple binding sites of the tetramer.

Amino Acid Sequence↗

Influenza and the rates of hospitalization for respiratory disease among infants and young children.

BACKGROUND: Young children may be at increased risk for serious complications from influenzavirus infection. However, in population-based studies it has been difficult to separate the effects of influenzavirus from those of respiratory syncytial virus. Respiratory syncytial virus often circulates with influenzaviruses and is the most frequent cause of hospitalization for lower respiratory tract infections in infants and young children. We studied the rates of hospitalization for acute respiratory-disease among infants and children during periods when the circulation of influenzaviruses predominated over the circulation of respiratory syncytial virus. METHODS: For each season from October to May during the period from 1992 to 1997, we used local viral surveillance data to define periods in Washington State and northern California when the circulation of influenzaviruses predominated over that of respiratory syncytial virus. We calculated the rates of hospitalization for acute respiratory disease, excess rates attributable to influenzavirus, and incidence-rate ratios for all infants and children younger than 18 years of age who were enrolled in either the Kaiser Permanente Medical Care Program of Northern California or the Group Health Cooperative of Puget Sound. RESULTS: The rates of hospitalization for acute respiratory disease among children who did not have conditions that put them at high risk for complications of influenza (e.g., asthma, cardiovascular diseases, or premature birth) and who were younger than two years of age were 231 per 100,000 person-months at Northern California Kaiser sites (from 1993 to 1997) and 193 per 100,000 person-months at Group Health Cooperative sites (from 1992 to 1997). These rates were approximately 12 times as high as the rates among children without high-risk conditions who were 5 to 17 years of age (19 per 100,000 person-months at Northern California Kaiser sites and 16 per 100,000 person-months at Group Health Cooperative sites) and approached the rates among children with chronic health conditions who were 5 to 17 years of age (386 per 100,000 person-months and 216 per 100,000 person-months, respectively). CONCLUSIONS: Infants and young children without chronic or serious medical conditions are at increased risk for hospitalization during influenza seasons. Routine influenza vaccination should be considered in these children.

Acute Disease↗

Decreased antibody response among nursing home residents who received recalled influenza vaccine and results of revaccination, 1996-97.

In November 1996, 11 lots of one U.S. manufacturer's 1996-97 trivalent influenza vaccine were voluntarily recalled because of decreasing potency of the A/Nanchang/933/95 (H3N2) component. Because the elderly are at high risk of developing influenza-related complications, we assessed the postvaccination antibody titers of nursing home residents who received recalled vaccine and assessed the antibody response to revaccination. Blood samples were collected 3 weeks after vaccination from 86 residents at three nursing homes who received recalled vaccine and 86 residents at three other nursing homes who received a different manufacturer's vaccine. Medical records were reviewed. Residents of one nursing home were later revaccinated. Blood samples were collected on the day of revaccination and again in 3 weeks. Serum was tested by hemagglutination inhibition for antibody to all three components of the 1996-97 influenza vaccine. The geometric mean antibody titer (GMT) (33 vs 55; p=0.01) and the percentage of residents with an antibody titer > or = 1:40 (52 vs 67%; p=0.04) to the A/Nanchang/933/95 component were lower among residents who received recalled vaccine compared to those who received non-recalled vaccine, but had similar GMTs against the other two vaccine components. After revaccination, the GMT to A/Nanchang/933/95 increased from 24 on the day of revaccination to 39 (p=0.01) in residents from one nursing home. Therefore, vaccination with the recalled vaccine was associated with lower postvaccination antibody titers to A/Nanchang/933/95, but not against the other two vaccine components. Revaccination was moderately effective in increasing antibody titers. With annual changes in influenza vaccine strains, routine post-release stability testing of influenza vaccine should continue.

Aged↗

TT virus infection in patients with chronic liver disease of unknown etiology.

The role of a novel virus, designated as TT virus (TTV), as a cause of chronic liver disease has not been well defined. We investigated the prevalence of TTV among 69 patients with chronic liver disease of unknown etiology and 50 volunteer blood donors with normal transaminase levels. TTV DNA was amplified by polymerase chain reaction (PCR) by using two different sets of primers: one based on the sequence of the original N22 clone within the open reading frame 1 (set A) and the other derived from the untranslated region (set B). The prevalence of TTV detected by PCR primers set A only, set B only, and in total (by either set A or B) was 11 (31%), 31 (86%), and 31 (86%) of 36 patients with chronic hepatitis; 2 (40%), 4 (80%), and 4 (80%) of 5 with cirrhosis; 11 (39%), 17 (61%), and 22 (79%) of 28 with hepatocellular carcinoma; and 9 (18%), 39 (78%), and 40 (80%) of 50 volunteer blood donors, respectively. Of the interpretable 25 PCR products amplified with primers set A, 9 were classified as genotype 1a, 10 as genotype 1b, 4 as genotype 2, 1 as genotype 3, and 1 as genotype 4. Molecular evolutionary analysis did not suggest any particular strains of TTV that might be associated with chronic liver disease. The nucleotide sequences of the untranslated region on which PCR primers set B were designed were highly conserved, and the interpretable 22 PCR products amplified with primers set B were not clearly divisible into distinct genotypes. Our findings provided no evidence that TTV is a causative agent of chronic liver disease.

Chronic Disease↗

Telomere sequences attached to nuclearly migrated yeast linear plasmid.

The yeast linear plasmid pCLU1, derived from pGKL1, has terminal proteins (TPs) covalently attached at the 5' ends of inverted terminal repeats (ITRs) and replicates in the cytoplasm, presumably using the TP as a primer for DNA synthesis. In Saccharomyces cerevisiae, under certain conditions, pCLU1 migrated into the nucleus and replicated in either linear or circular form. The linear-form plasmid lacked TPs; instead it carried host-telomere repeats at the ITR ends. The present study showed that (1) the added telomere was primarily composed of the repeated tracts of TGTGTGGGTGTGG, which was complementary to the RNA template of yeast telomerase, (2) the telomeric addition occurred at the very end of the ITRs, and (3) the sequence composition of the added telomeres was diverse among individual plasmids, but symmetrically identical at both ends of each plasmid. A similar mode of telomere addition was also observed in cells defective in the RAD52 gene.

Base Sequence↗

[Cardiac imaging with rapid, retrospective ECG synchronized multilevel spiral CT].

PURPOSE: In this paper a method for cardiac imaging with fast multi-slice CT and retrospectively ECG-gated spiral acquisition is presented. METHODS: A fast multi-slice CT system with 4 simultaneously acquired slices and 0.5 s rotation time is used (Siemens Somatom VolumeZoom). Continuous spiral data of the entire heart volume is acquired together with the patient's ECG and reconstructed with dedicated spiral algorithms providing 250 ms temporal resolution. Three-dimensional image data sets are built up from overlapping slices that are reconstructed in an arbitrary, user-defined phase of the heart cycle (e.g. diastolic phase). To evaluate the capability of the method for functional imaging complete three-dimensional image volumes are reconstructed from the same spiral data set in different phases of the heart cycle. RESULTS: A spiral data set of the entire heart volume may be acquired within a single breath-hold. Typical scan times for standard examinations with 3 mm slice width are 10-15 s, and for high-resolution CT angiographies of the coronary arteries with 1.25 mm slice width about 30-35 s. Motion-free reconstruction of the heart and coronary arteries with high spatial resolution is possible in the diastolic phase of the heart cycle. Multi-phase reconstructions from the same spiral scan data set are possible, however, motion artifacts in heart phases with fast cardiac motion may not be completely avoided. CONCLUSION: Fast multi-slice spiral CT with retrospectively ECG-gated spiral reconstruction is well suited for three-dimensional and functional imaging of the heart, especially for high-resolution imaging of calcified coronary plaques and CT-angiography of the coronary arteries.

Algorithms↗

Purification and characterization of isoamyl acetate-hydrolyzing esterase encoded by the IAH1 gene of Saccharomyces cerevisiae from a recombinant Escherichia coli.

The IAH1 gene of Saccharomyces cerevisiae encodes an esterase that preferentially acts on isoamyl acetate; however, the enzyme has not yet been completely purified from the yeast S. cerevisiae. We constructed the IAH1 gene expression system in Escherichia coli, and purified the IAH1 gene product (Iah1p). The amount of Iah1p produced by recombinant E. coli was more than 40% of total cellular proteins. The molecular size of Iah1p was 28 kDa by SDS-polyacrylamide gel electrophoresis. Judging from the molecular weight estimation by gel filtration of purified Iah1p, the enzyme was thought to be a homodimer. The Km values for isoamyl acetate and isobutyl acetate were 40.3 mM and 15.3 mM, respectively. The enzyme activity was inhibited by Hg2+, p-chloromercuribenzoate, and diisopropylfluorophosphate.

Carboxylic Ester Hydrolases↗

Partial purification and characterization of thermostable acid phosphatase from thermoacidophilic archaeon Sulfolobus acidocaldarius.

Thermostable acid phosphatase (APase) from thermoacidophilic archaeon Sulfolobus acidocaldarius was isolated, partially purified, and characterized. The optimum pH and temperature of the enzyme for p-nitrophenylphosphate (pNPP) as a substrate were 5.0 and 70 degrees C, respectively. The apparent K(m) value was 1.9 mM. This APase showed a native molecular mass of 20 kDa on a gel filtration chromatography. Of the APase activity, 60% remained after 60 min of heat treatment at 75 degrees C. To confirm whether the APase is active in the monomeric form, we attempted to elute the enzyme from SDS-polyacrylamide gels with Disk electrophoresis apparatus and renature the enzyme. The APase activity was recovered up to 50% in the 14- to 35-kDa range, and maximum around 25 kDa. These results suggest that this APase is monomeric protein.

Acid Phosphatase↗

Gallic acid induces vascular smooth muscle cell death via hydroxyl radical production.

In the present study, we investigated whether gallic acid (GA) can induce death in cultured vascular smooth muscle cells (VSMCs), and whether production of the hydroxyl radical (.OH) is involved in the process of GA action. GA killed cultured VSMCs from rat aorta, in a dosc- and time-dependent manner. Cytoplasmic shrinkage and nuclear condensation were observed light microscopically in GA-treated VSMCs, which appeared apoptotic. However, the ultrastructure of the VSMC was not typical of apoptosis: nuclear condensation was not glossy, and the plasma membrane and subccellular organelles were disrupted. Although the VSMC were positive for in situ nick end-labeling (TUNEL). they did not show a DNA ladder pattern on gel electrophoresis and were negative for T aq polymerase-based in situ ligation, which is more specific for apoptosis than TUNEL. Moreover. GA-induced cell death was not prevented by Boc-Asp-fmk (a pan-caspase inhibitor). Production of OH was detected in GA-treated VSMCs using high-performance liquid chromatography with salicylic acid as a trapping agent. Lipid peroxidation was also observed. The production of .OH was inhibited by catalase (CAT) and deferoxamine (DFX), and these treatments completely rescued VSMCs from cell death. In a cell-free system, GA produced .OH in the presence of Fe2+-EDTA, which was quenched by CAT and DFX, suggesting involvement of the Haber-Weiss reaction. Oxidative stress by reactive oxygen species, .OH in particular, is one of the mechanisms of GA-induced death of VSMCs, the mode of which was different from typical apoptosis.

Animals↗

Relocation of a cytoplasmic yeast linear plasmid to the nucleus is associated with circularization via nonhomologous recombination involving inverted terminal repeats.

The linear plasmid pCLU1 from the yeast Kluyveromyces lactis normally replicates in the cytoplasm, with the aid of the helper linear plasmid pGKL2, using terminal protein (TP) as a primer. However, it relocates to the nucleus when selection is applied for the expression of a plasmid-borne nuclear marker. Migration to the nucleus occurred in K. lactis at a frequency of about 10(-3)/cell ten or more times higher than the rate observed in Saccharomyces cerevisiae. The nuclear plasmids existed only in a circularized form in K. lactis, while in S. cerevisiae a telomere-associated linear form is also found. Sequence analysis showed that circularization in K. lactis was caused by non-homologous recombination between the inverted terminal repeat (ITR) at the ends of the linear form and non-specific internal target sites in pCLU1. No sequence similarity existed among the junction sites, indicating that the free ITR end plays a crucial role in circularization. In S. cerevisiae, circular plasmids were generated not only by nonhomologous recombination, but also by homologous recombination between short direct repeats within pCLU1. Circularization via the ITR end was observed independently of RAD52 activity. Sequences highly homologous to ARS core elements, 5'-ATTTATTGTTTT-3' for K. lactis and 5'-(A/T)TTTAT(T/G)TTT(A/T)-3' for S. cerevisiae, were detected at multiple sites in the nuclear forms of the plasmids.

Base Sequence↗

Does anovulation induced by oral contraceptives favor pregnancy during the following two menstrual cycles?

OBJECTIVE: To compare IVF and pregnancy outcomes before and after anovulation induced by oral contraceptives. DESIGN: Observational clinical study. SETTING: Infertility clinic. PATIENT(S): Forty women with two intact ovaries (32 of 40 couples with male factor infertility and 8 with unknown causes of infertility) underwent 190 IVF treatment cycles (55 natural cycles and 135 clomiphene citrate-stimulated cycles). INTERVENTION(S): If the women failed to conceive after 2-4 IVF treatment cycles, oral contraceptives were used to induce anovulation for 1 month before IVF was performed in two consecutive cycles. MAIN OUTCOME MEASURE(S): Rates of oocyte retrieval, fertilization, cleavage, preembryo formation, pregnancy, and implantation were compared before and after a period of anovulation. RESULT(S): The pregnancy rate per cycle of the first and second cycle combined (23%) and that of the second cycle alone (30%) after a period of anovulation were significantly higher than that observed before a period of anovulation (9%). CONCLUSION(S): Anovulation induced by oral contraceptives, showing bilateral ovarian quiescence, enhances pregnancy rates in the following two menstrual cycles of IVF treatment.

Adult↗

Genipin, a metabolite derived from the herbal medicine Inchin-ko-to, and suppression of Fas-induced lethal liver apoptosis in mice.

BACKGROUND & AIMS: We showed previously that a Kampo (Chinese/Japanese herbal) medicine, Inchin-ko-to (ICKT), inhibits hepatocyte apoptosis induced by transforming growth factor beta1 in vitro. The present study investigated whether ICKT or its ingredients inhibit Fas-mediated liver apoptosis in vivo. METHODS: Acute liver injury was induced by an intravenous injection of anti-Fas antibody, Jo2. The effects of ICKT and its ingredients on lethality, histology, apoptotic index, serum transaminase levels, caspase activation, mitochondrial membrane potential (Deltapsi(m)), and mitochondrial permeability transition (MPT) were analyzed. Apoptosis in mouse hepatocytes in vitro was also evaluated. RESULTS: Pretreatment with ICKT rescued 75% of Jo2-treated mice and markedly suppressed liver apoptosis/injury. Genipin, an intestinal bacterial metabolite of geniposide that is a major ingredient of ICKT, was found to be an active principle of ICKT. Genipin also suppressed in vitro Fas-mediated apoptosis in primary-cultured murine hepatocytes. Activation of caspase 3 and 8 in the liver homogenate and rapid reduction of triangle uppsi(m) of hepatocytes isolated from Jo2-treated mice were inhibited by genipin preadministration. The resistance to Ca(2+)-induced MPT was enhanced in liver mitochondria of genipin-treated mice. CONCLUSIONS: These results suggest that the antiapoptotic activity of genipin via the interference with MPT is a possible mechanism for therapeutic effects of ICKT.

Alanine Transaminase↗