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Biomedical subjects

H Niki

Publications and source records attributed to H Niki.

At least 91 records · Page 5Linked to original sources
PubMed1990

Influenza antibody titers after vaccination of chronic renal failure patients; before and during hemodialysis, or on continuous ambulatory peritoneal dialysis.

Anti-influenza antibody (Ab) titers were measured in order to elucidate whether there are any disturbances in Ab production in chronic renal failure (CRF) patients. A total of 55 CRF patients plus 15 normal individuals were vaccinated with influenza vaccine twice, 4 weeks apart of the 55 CRF patients, 15 were not on dialysis, 10 were undergoing hemodialysis (HD), and 30 were on continuous ambulatory peritoneal dialysis (CAPD). Of the 30 CAPD patients, 14 had peritonitis. Serum Ab titers were measured by complement fixation (CF) and hemagglutination inhibition (HI) tests, and IgG and IgM class specific antibodies by ELISA. All groups responded to immunization, but CAPD patients with peritonitis and CRF patients not yet on dialysis did not show a significant elevation in IgM class Ab titers. The number of CAPD patients with peritonitis who achieved positive titers was significantly lower in HI (p less than 0.01) and IgG class antibodies (p less than 0.05) compared with normal controls. Two patients with frequent peritonitis did not show any response to vaccination. It was concluded that patients with renal dysfunction have some abnormalities in Ab production against influenza vaccine, the effects of which were more pronounced in the CAPD patients with frequent peritonitis.

Adolescent↗
PubMed1989

Purification and characterization of SopA and SopB proteins essential for F plasmid partitioning.

Mini-F plasmid has the trans-acting genes sopA and sopB and the cis-acting site sopC which are essential for accurate partitioning of plasmid DNA molecules into both daughter cells. In this study, we purified independently SopA and SopB proteins, analyzed the in vitro DNA-binding activity of these proteins by the gel retardation assay, and determined the precise binding sites of DNA by the footprinting method. SopA binds to four repeated sequences (CTTTGC) located in the promoter-operator region of the sopAB operon. The SopA binding activity is enhanced by the addition of SopB protein. SopB protein itself does not bind to this DNA region. These results suggest that the complex of SopA and SopB proteins autoregulate the expression of the sopA-sopB operon. On the other hand, SopB protein binds to the sopC region, in which 12 direct repeats of 43-base pairs nucleotides exist. SopB protein recognizes the inverted repeats of 7 base pairs in each direct repeats. SopA protein does not affect the SopB binding activity to the sopC DNA segment.

Bacterial Proteins↗
PubMed1989

Involvement of DnaK protein in mini-F plasmid replication: temperature-sensitive seg mutations are located in the dnaK gene.

The seg mutants (seg-1 and seg-2) of Escherichia coli cannot support the replication of the F factor and mini-F plasmids at 42 degrees C. We cloned the wild-type E. coli chromosomal DNA fragment complementing the seg-1 and seg-2 mutations and found that both mutations were complemented by the wild-type dnaK gene coding for a heat shock protein. Transduction with phage P1 indicated that the seg-2 mutation is located at about 0.3 min in the region containing the dnaK gene in the order trpR--thrA--seg-2--leuB, consistent with the locus of the dnaK gene. Cloning and sequencing of the dnaK gene of the seg mutants showed that there was one base substitution within the dnaK gene in each mutant causing an amino acid substitution. These results indicate that the seg gene in which the seg-1 and seg-2 mutations occurred is identical to the dnaK gene. The mini-F plasmid pXX325 did not transform a dnaK null mutant to ampicillin resistance at 30 degrees C in contrast to plasmids pBR322, pACYC184 and pSC101, which did. The active dnaK (seg) gene product is therefore essential for replication of the mini-F plasmid at both 30 degrees and 42 degrees C.

Bacterial Proteins↗
PubMed1989

Insulin release by D-glucose anomers in a non-insulin-dependent diabetes rat model.

The alpha anomer of D-glucose is more potent than the beta anomer in stimulating insulin release. We have studied the effects of D-glucose anomers on insulin release from the perfused pancreas isolated from a rat model of non-insulin-dependent diabetes (NIDD) induced by streptozotocin injection at 2 days of age. Insulin release from the pancreas of the diabetic rat in response to 10 mM alpha-D-glucose was markedly impaired, while insulin response to the same concentration of beta-D-glucose was only slightly reduced as compared to that in the control pancreas. Thus, the pancreatic B cell of the diabetic rat did not discriminate between the alpha and beta anomers of D-glucose. Insulin release induced by 5 mM D-glyceraldehyde was decreased in the diabetic pancreas, while insulin release induced by 0.15 mg/ml tolbutamide did not differ from that in the control pancreas. Glucose oxidation in the islets isolated from the diabetic pancreas was not lower than that in comparable control islets. Treatment of the diabetic pancreas with 5 microM forskolin or 0.15 mg/ml tolbutamide did not restore its defective discrimination between the two anomers, although forskolin potentiated insulin release more markedly in the diabetic pancreas. The findings may provide some insight into the pathophysiology of the pancreatic B cell in NIDD.

Animals↗
PubMed1989

Identification of human apolipoprotein E variant gene: apolipoprotein E7 (Glu244,245----Lys244,245).

Apolipoprotein E (apoE) is one of the protein moieties of the human serum lipoproteins. Three major isoforms of apoE (apoE2, apoE3, and apoE4) and minor variant isoforms (apoE1, apoE5, and apoE7) have been detected by isoelectric focusing. In this study we have cloned the apoE7 gene from a patient with the apoE3/E7 phenotype associated with hypertriglyceridemia and diabetes mellitus. DNA sequencing revealed that the apoE7 gene has two base substitutions (G----A) changing Glu244,245----Lys244,245, compared with the apoE3 gene. The replacement of the two amino acids is consistent with the result of isoelectric focusing of the apoE7 isoprotein, which shifts to four positively charged units compared with the apoE3 isoprotein.

Amino Acid Sequence↗
PubMed1989

Molecular cloning of a human apolipoprotein E variant: E5 (Glu3----Lys3).

Two types of apoE alleles from a genomic DNA library of a subject with the apoE2/E5 phenotype have been cloned. One of these alleles encodes an apoE isoprotein having cysteine, arginine, and cysteine at positions 112, 145, and 158 of mature apoE isoproteins, respectively, indicating an epsilon apoE2 allele. The other allele encodes a different isoprotein, having cysteine, arginine, and arginine at each of the above positions, respectively. In addition, this allele has a base substitution (G----A) which causes the substitution of lysine for glutamic acid at position 3 near the NH2-terminus of the mature apoE. This allele is a new variant, the epsilon apoE5 allele.

Amino Acid Sequence↗
PubMed1989

Chromosome partitioning in Escherichia coli: novel mutants producing anucleate cells.

To study the chromosomal partitioning mechanism in cell division, we have isolated a novel type of Escherichia coli mutants which formed anucleate cells, by using newly developed techniques. One of them, named mukA1, is not lethal and produces normal-sized anucleate cells at a frequency of 0.5 to 3% of total cells in exponentially growing populations but does not produce filamentous cells. Results suggest that the mutant is defective in the chromosome positioning at regular intracellular positions and fails frequently to partition the replicated daughter chromosomes into both daughter cells, resulting in production of one anucleate daughter cell and one with two chromosomes. The mukA1 mutation causes pleiotropic effects: slow growth, hypersensitivity to sodium dodecyl sulfate, and tolerance to colicin E1 protein, in addition to anucleate cell formation. Cloning of the mukA gene indicates that the mukA1 mutation is recessive and that the mukA gene is identical to the tolC gene coding for an outer membrane protein.

Bacterial Outer Membrane Proteins↗
PubMed1989

Penicillin-binding protein 2 is essential in wild-type Escherichia coli but not in lov or cya mutants.

Penicillin-binding protein 2 (PBP2), target of the beta-lactam mecillinam, is required for rod morphology and cell wall elongation in Escherichia coli. A new temperature-sensitive PBP2 allele and an in vitro-constructed insertion deletion allele were shown to be lethal in wild-type strains, establishing that the activity of this protein is essential. Mutations in the lov or cya genes, conferring mecillinam resistance, compensated for the deleterious effect of the absence of PBP2. The resulting double mutants grew as spheres. In a cya mutant lacking PBP2, the restoration of a Cya+ phenotype by addition of cyclic AMP caused lethality and a block in cell division. These results show that in wild-type cells, PBP2 is essential for growth and division.

Acyltransferases↗
PubMed1989

Activity of hippocampal formation neurons in the monkey related to a conditional spatial response task.

To analyze neurophysiologically the functions of the primate hippocampus, the activity of 905 single hippocampal formation neurons was analyzed in two rhesus monkeys performing a conditional spatial response task known to be impaired in monkeys and in man by damage to the hippocampus or fornix. In the task, the monkey learned to make one spatial response, touching a screen three times when he saw one visual stimulus on the video monitor, and a different spatial response, of withdrawing his hand from the screen, when a different visual stimulus was shown. Fourteen percent of the neurons fired differentially to one or the other of the stimulus-spatial response associations. The mean latency of these differential responses was 154 +/- 44 (SD) ms. The firing of these neurons was shown to reflect a combination of the particular stimulus and the particular response associated by learning in the stimulus-response association task and could not be accounted for by the motor requirements of the task, nor wholly the stimulus aspects of the task, as demonstrated by testing their firing in related visual discrimination tasks. Responsive neurons were found throughout the hippocampal formation, but were particularly concentrated in the subicular complex and the CA3 subfield. These results show that single hippocampal neurons respond to combinations of the visual stimuli and the spatial responses with which they must become associated in conditional spatial response tasks and are consistent with the suggestion that part of the mechanism of this learning involves associations between visual stimuli and spatial responses learned by single hippocampal neurons.

Action Potentials↗
PubMed1989

Receptors of paraneurons, with special reference to glucoreceptors.

Among glucose-recognizing paraneurons, the gustatory cell is believed to have a glucoreceptor, while the pancreatic B cell is thought to metabolize glucose for signal production for insulin release. To investigate whether a common mechanism of glucose recognition exists among these cells, we have studied the interaction of the anomers of glucose or its derivative, known as a sugar taste inhibitor, with the pancreatic B cell of normal and diabetic rats. Inhibitors of the sugar taste response inhibited glucose-induced insulin release in various manners. A non-specific inhibitor, dibucaine, impaired not only the insulin response to glucose but also the ability to discriminate the anomers of glucose, without inhibiting glucose oxidation in the islets. Dibucaine also inhibited insulin release induced by a non-glucose secretagogue, tolbutamide. The alpha anomer, but not the beta anomer, of p-nitrophenyl-D-glucopyranoside, a specific-competitive inhibitor of sugar taste response, inhibited glucose-induced insulin release, but did not inhibit insulin release induced by non-glucose secretagogues or glucose oxidation. The pancreatic B cell of a non-insulin-dependent diabetes (NIDD) rat model, the NSZ rat, exhibited low insulin response to glucose and did not discriminate between the two anomers of glucose. The diabetic B cell responded to non-glucose secretagogues to the same extent as the control. Glucose oxidation in the diabetic islets was not impaired. These findings, together with previous ones, suggest that the gustatory and pancreatic B cells have a common glucose recognition site, which has a steric preference for the alpha anomer and is impaired in NIDD.

Animals↗
PubMed1989

Hippocampal neurons in the monkey with activity related to the place in which a stimulus is shown.

In order to analyze the functions of the hippocampus in the primate, and to advance the understanding of amnesia, the activity of 994 single hippocampal neurons in the monkey was analyzed during the performance of a task known to be affected by hippocampal damage in which both an object, and its position in space, must be remembered. The serial multiple object-place memory task required a memory for the position on a video monitor in which a given object had appeared previously. It was found that 9.3% of neurons recorded in the hippocampus and hippocampal gyrus had spatial fields in this and related tasks, in that they responded whenever there was a stimulus in some but not in other positions on the screen. We found that 2.4% of the neurons responded to a combination of spatial information and information about the object seen, in that they responded more the first time a particular object was seen in any position. Six of these neurons were found that showed this combination even more clearly, in that, for example, they responded only to some positions and only if it was the first time that a particular stimulus had appeared there. It is concluded that there are neurons in the primate hippocampus which (1) respond to position in space and (2) in some cases combine information about stimuli and their position in space, responding to a stimulus only the first time it is seen in a position in space, for example. Thus, not only is spatial information processed by the primate hippocampus, but it can be combined with information about which stimuli have been seen before. The ability of the hippocampus to form such conjunctions may be an important property for its role in memory.

Analysis of Variance↗
PubMed1988

Insulin release by glucose anomers in a rat model of non-insulin-dependent diabetes.

The effects of the alpha and beta anomers of D-glucose on insulin release were studied in a rat model of non-insulin-dependent diabetes, which was induced by streptozotocin injection at 2 days of age. Glucose tolerance of the streptozotocin-treated rats at 8-10 weeks of age was mildly diabetic. Insulin release from the isolated perfused pancreas of the diabetic rats in response to 10 mmol/l alpha-D-glucose was markedly impaired, while insulin response to 10 mmol/l beta-D-glucose in the diabetic pancreas was only slightly reduced as compared to that in the control pancreas.

Animals↗
PubMed1988

Chromosomal genes essential for stable maintenance of the mini-F plasmid in Escherichia coli.

We have isolated mutants of Escherichia coli which do not support stable maintenance of mini-F plasmids (delta ccd rep+ sop+). These host mutations, named hop, were classified into five linkage groups on the E. coli chromosome. Genetic analyses of these hop mutations by Hfr mating and P1 transduction showed their loci on the E. coli genetic map to be as follows: hopA in the gyrB-tnaA region, hopB in the bglB-oriC region, hopD between 8 and 15 min, and hopE in the argA-thyA region. Kinetics of stability of the sop+ and delta sop mini-F plasmids in these hop mutants suggest that the hopA mutants are defective in partitioning of mini-F rather than in plasmid replication. The hopB, hopC, and hopD mutants were partially defective in replication of mini-F. The physical structure of the plasmid DNA was normal in hopA, B, C, and D mutants. Large amounts of linear multimers of plasmid DNA accumulated in mutants of the fifth linkage group (hopE). None of the hop mutations in any linkage group affected the normal growth of cells.

Alleles↗
PubMed1988

Possible involvement of diacylglycerol-activated, Ca2+-dependent protein kinase in glucose memory of the rat pancreatic B-cell.

Exposure to high concentrations of glucose potentiates insulin release from the pancreatic B-cell stimulated by various secretagogues after an interval under basal condition. We studied the role of diacylglycerol-activated, Ca2+-dependent protein kinase (protein kinase C) in this priming effect of glucose in rat pancreatic islets, using 12-O-tetradecanoyl phorbol-13-acetate (TPA), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7),N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) and forskolin. The priming effect of glucose was mimicked by 10 nmol/l of TPA, an activator of protein kinase C, but not by 5 mumol/l of forskolin, which increases cAMP via activating adenylate cyclase. When pancreatic islets were exposed to glucose (10 mmol/l) together with 50 mumol/l of H-7, an inhibitor of protein kinase C, the secretory response to glucose (10 mmol/l) after a 30-min interval was significantly reduced compared with that in the islets previously exposed to 10 mmol/l glucose alone. In contrast, this was not the case for HA-1004, its inhibitory activity against protein kinase C being less potent than H-7. These findings suggest that protein kinase C may play an important role in the priming effect of glucose on the pancreatic B-cell.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗