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Biomedical subjects

Noriko Tamura

Publications and source records attributed to Noriko Tamura.

At least 19 recordsLinked to original sources
PubMed2007

Urinary retention and sympathetic sphincter obstruction in axonal Guillain-Barré syndrome.

A 62-year-old woman with axonal Guillain-Barré syndrome developed weakness and urinary retention simultaneously. The retention failed to recover for 10 months even after she regained the ability to walk. The patient exhibited no postural hypotension. Videourodynamics showed that the retention was caused not by the bladder paralysis but rather by internal (sympathetic) sphincter obstruction, which is extremely uncommon in peripheral neuropathies. We started the patient on an alpha-adrenergic antagonist, urapidil, at 30 mg/day, and this led to successful relaxation of the urethra and reduced the postvoid residual from 200 ml to less than 30 ml. The underlying mechanisms of urinary retention in our patient appeared to involve hyperactive lumbosacral sympathetic nerves. Urinary retention and sympathetic sphincter obstruction can thus be features of axonal Guillain-Barré syndrome.

Adrenergic alpha-Antagonists↗
PubMed2007

Time course of axonal regeneration in acute motor axonal neuropathy.

Patients with acute motor axonal neuropathy (AMAN) generally recover well. We reviewed clinical and electrophysiologic recovery in 13 patients for up to 5 years. Twelve patients showed rapid recovery over 12 months, whereas in the remaining one the recovery was slow and incomplete at 5 years. In AMAN, axonal degeneration appears to develop predominantly in the motor nerve terminals, and only occasionally more proximally in the nerve roots. Nerve terminal degeneration-regeneration presumably provides a mechanism for good recovery.

Adolescent↗
PubMed2006

The effects of physiological fluctuation of serum potassium levels on excitability properties in healthy human motor axons.

OBJECTIVE: Previous axonal excitability studies suggest hyperkalemia or hypokalemia can significantly alter membrane potential and thereby, excitability properties. We studied whether physiological fluctuation of serum potassium levels affects axonal excitability in normal human axons. METHODS: Threshold tracking was used to measure strength-duration properties, refractory periods, supernormality, and threshold electrotonus in median motor axons of 12 normal volunteers. In each subject, the excitability indices and serum potassium levels were measured three times (baseline, 2h later, and 2 weeks later). RESULTS: The pooled data (n=36) showed significant correlation of the relative refractory period, supernormality, and depolarizing threshold electrotonus with potassium levels. Among each trial (12 subjects) the correlation did not reach statistical significance occasionally. Strength-duration properties, refractoriness, late subnormality, and hyperpolarizing threshold electrotonus were not significantly affected by serum potassium levels. CONCLUSIONS: Even in the normal range, serum potassium levels could slightly alter axonal excitability of human axons. Among excitability indices, the relative refractory period, supernormality, and threshold electrotonus are sensitive to potassium levels. SIGNIFICANCE: Physiological fluctuation of serum potassium levels could partly be responsible for inter- and intra-subject variability of excitability indices.

Adult↗
PubMed2006

A multipurpose transposon-based vector system mediates protein expression in Rhodococcus erythropolis.

In the current study we developed two transposon-based vectors; namely pTNR-KA and pTNR-TA and utilized them for expression of proteasome complex, derived from Streptomyces coelicolor, in Rhodococcus erythropolis. The two vectors can be transposed into Rhodococcus cells by means of electroporation, either individually in two consecutive processes or in combinations by a single step. During transposition, each of the two vectors liberates its transposable-marker gene, which integrated in a single copy into a random site in the Rhodococcus chromosomal DNA. Southern blot analysis indicated that the two transposable-marker genes of both vectors does not alter or knock out each other. To utilize these vectors for Streptomyces proteasome expression, two expression cassettes were constructed; each cassette comprised a constitutive promoter (P(nit)), the DNA fragment, prcA or prcB that encodes alpha- or beta-subunits of Streptomyces proteasome, and T(thcA) transcriptional terminator. The cassettes were then individually introduced into the multiple cloning sites that are located in the transposable-marker gene of the two vectors. The two cassettes-harboring vectors were subsequently co-transposed, in combinations, into the Rhodococcus genome by a single electroporation step and the Streptomyces proteasome was successfully expressed in the rodococcal host cell. The isolated proteasome was further characterized and the peptidase activity was confirmed and indicated that it was biologically active. The present study concluded that both pTNR-KA and pTNR-TA can be used as transposon-based protein expression systems in Rhodococcus species.

Animals↗
PubMed2006

Increased nodal persistent Na+ currents in human neuropathy and motor neuron disease estimated by latent addition.

OBJECTIVE: To investigate the changes in nodal persistent Na(+) currents in human neuropathy and motor neuron disease. In human motor axons, approximately 1.0% of total Na(+) channels are active at rest, termed "persistent" Na(+) channels, and the conductance can be non-invasively estimated by the technique of latent addition in vivo. METHODS: Latent addition was performed in median motor axons of 93 patients with axonal neuropathy (n=38), lower motor neuron disorder (LMND; n=19) or amyotrophic lateral sclerosis (ALS; n=36) and in 27 age-matched normal subjects. Brief hyperpolarizing conditioning current pulses were delivered, and threshold change at the conditioning-test interval of 0.2 ms was measured as an estimator of the magnitude of persistent Na(+) currents. Threshold electrotonus and supernormality were also measured as indicators of resting membrane potential. RESULTS: Threshold changes at 0.2 ms were significantly greater in patients with neuropathy or LMND (p<0.05), and tended to be greater in ALS patients (p=0.075) than in normal controls. Threshold electrotonus and supernormality did not differ in each patient group and normal controls, suggesting that membrane potential is not altered in patients. In the recovery phase of axonal neuropathy, the threshold changes increased in parallel with an increase in amplitudes of compound muscle action potential. CONCLUSIONS: Persistent Na(+) currents appear to increase commonly in disorders involving lower motor neurons, possibly associated with axonal regeneration or collateral sprouting or changes in Na(+) channel gating. SIGNIFICANCE: The increased axonal excitability could partly be responsible for positive motor symptoms such as muscle cramping frequently seen in lower motor neuron disorders.

Action Potentials↗
PubMed2006

Isolation and characterization of high temperature-resistant germination mutants of Arabidopsis thaliana.

Temperature is a primary environmental cue for seed germination of many weeds and vegetables. To investigate the mechanism of germination regulation by temperature, we selected five high temperature (thermoinhibition)-resistant germination mutants (TRW lines) from 20,000 T-DNA insertion lines of Arabidopsis. Segregation analyses indicated that each of the five lines had single locus recessive mutations. The seeds of TRW134-15 and TRW187 showed reduced sensitivity to ABA and also to the gibberrellin biosynthesis inhibitor, paclobutrazol. Genetic and nucleotide sequencing analyses indicated that TRW187 is a new allele of abi3 (abi3-14). TRW71-1 exhibited a maternal effect for both thermoinhibition-resistant and transparent testa phenotypes, and genetic analysis revealed that the mutation was allelic to tt7 (tt7-4 sib). Interestingly, the seeds of reduced dormancy mutants rdo1, rdo2, rdo3 and rdo4 were also thermoinhibition tolerant, and all the TRW seeds showed reduced dormancy. Like rdo3, TRW13-1 had shorter siliques and slightly shorter stems than the wild type. The mutation of TRW13-1 was mapped to the bottom arm of chromosome 1 where rdo3 has also been mapped, but the two mutants are not allelic. We designated TRW13-1 as thermoinhibition-resistant germination 1 (trg1). We also mapped the ABA-insensitive mutation of TRW134-15 to the bottom arm of chromosome 5 and named it trg2. These results show that both embryo/endosperm and maternal factors contribute to germination inhibition at supraoptimal temperatures in Arabidopsis. In addition, we confirm the role of ABA in thermoinhibition of seed germination and a link between seed physiological dormancy and response to high temperature.

Abscisic Acid↗
PubMed2006

Distal excitability changes in motor axons in amyotrophic lateral sclerosis.

OBJECTIVE: Previous axonal excitability studies in amyotrophic lateral sclerosis (ALS) have suggested that impaired potassium channel function could be responsible for the generation of fasciculations, but the ectopic activity arises predominantly from the motor nerve terminals. This study tested the hypothesis that dysfunction of potassium channels is more pronounced in the more distal parts of axons. METHODS: Threshold electrotonus was used to compare accommodation at the motor point of abductor pollicis brevis, and at the wrist portion of the median nerve, between 22 patients with ALS and 19 normal subjects. As target responses for motor point stimulation, movement-related potentials were recorded using an accelerometer. RESULTS: Compared to normal subjects, ALS patients showed greater threshold changes to depolarizing conditioning currents at both the motor point and wrist, suggesting less accommodation by potassium currents. Differences in the threshold electrotonus curves between the normal and ALS groups were much more prominent at the motor point than at the wrist. CONCLUSIONS: In ALS, axonal potassium channels are impaired more prominently in distal portions of axons than at the nerve trunk, and this is consistent with evidence that fasciculations mostly arise from the nerve terminals. SIGNIFICANCE: Excitability testing at the motor point provides additional information about the pathophysiology of ALS.

Action Potentials↗
PubMed2006

Crystallization and preliminary crystallographic analysis of NAD+-preferring aldohexose dehydrogenase from the thermoacidophilic archaeon Thermoplasma acidophilum.

The aldohexose dehydrogenase from the thermoacidophilic archaeon Thermoplasma acidophilum (AldT) is a 28 kDa molecular-weight enzyme that catalyzes the oxidation of various aldohexoses, with a preference for NAD+ rather than NADP+ as a cofactor. The recombinant AldT was crystallized using the hanging-drop vapour-diffusion technique at 293 K under several acidic conditions with polyethylene glycol (PEG) and ammonium sulfate as precipitants. Optimization of the initial crystallizations conditions yielded single crystals in solution containing 0.1 M sodium acetate pH 4.6, 18%(w/v) PEG 4000, 0.2 M ammonium sulfate and 15%(v/v) glycerol. An X-ray diffraction data set was collected to a resolution of 2.8 A.

Archaeal Proteins↗
PubMed2006

Leucine-induced activation of translational initiation is partly regulated by the branched-chain alpha-keto acid dehydrogenase complex in C2C12 cells.

Branched-chain amino acid leucine has been shown to activate the translational regulators through the mammalian target of rapamycin. However, the leucine's effects are self-limiting because leucine promotes its own disposal by an oxidative pathway. The irreversible and rate-limiting step in the leucine oxidation pathway is catalyzed by the branched-chain alpha-keto acid dehydrogenase (BCKDH) complex. The complex contains E1 (alpha2beta2), E2, and E3 subunits, and its activity is abolished by phosphorylation of the E1alpha subunit by BCKDH kinase. The relationship between the activity of BCKDH complex and leucine-mediated activation of the protein translation was investigated using the technique of RNA interference. The activity of BCKDH complex in C2C12 cell was modulated by transfection of small interfering RNA (siRNA) for BCKDH E2 subunit or BCKDH kinase. Transfection of siRNAs decreased the mRNA expression and protein amount of corresponding gene. Suppression of either E2 subunit or kinase produced opposite effects on the cell proliferation and the activation of translational regulators by leucine. Suppression of BCKDH kinase for 48h resulted in decreasing cell proliferation. In contrast, E2 suppression led to increased amount of total cellular protein. The phosphorylation of p70 S6 kinase by leucine was increased in E2-siRNA transfected C2C12 cells, whereas the leucine's effect was diminished in kinase-siRNA transfected cells. These results suggest that the activation of the translational regulators by leucine was partly regulated by the activity of BCKDH complex.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2006

Latent addition in human motor and sensory axons: different site-dependent changes across the carpal tunnel related to persistent Na+ currents.

OBJECTIVE: To compare site-dependent changes across the carpal tunnel in axonal persistent Na+ conductances in motor and sensory axons. Positive sensory symptoms are prominent features in carpal tunnel syndrome, and a persistent Na+ current is a major determinant of axonal excitability. METHODS: The technique of latent addition was used to estimate persistent Na+ currents in median motor and sensory axons at the wrist and palm of 10 normal subjects. Brief hyperpolarizing conditioning current pulses were delivered, and threshold change at the conditioning-test interval of 0.2 ms was measured as an indicator of persistent Na+ currents. RESULTS: Threshold changes at 0.2 ms were greater in sensory than in motor axons at both the wrist and palm. In motor axons, the threshold changes were significantly smaller at the palm (mean, 4.9%) than at the wrist (10.0%). By contrast, the threshold changes were similar at the two sites of sensory axons (12.6 and 13.1%). The passive membrane time constant was similar for motor and sensory axons at the palm and wrist. CONCLUSIONS: Nodal persistent Na+ conductances have substantial site-dependent changes decreasing distally across the carpal tunnel in median motor axons, but not in sensory axons. SIGNIFICANCE: Whereas sensory axons generally have higher excitability than motor axons, the sensory-motor differences become more prominent across, and possibly at the carpal tunnel than the nerve trunk, and it is suggested that this contributes to the predominance of positive sensory symptoms in carpal tunnel syndrome.

Action Potentials↗
PubMed2006

Nodal persistent Na+ currents in human diabetic nerves estimated by the technique of latent addition.

OBJECTIVE: To investigate the effects of hyperglycemia on persistent Na+ currents in human diabetic nerves, eliminating the factors of passive membrane properties as a factor. Previous studies show that strength-duration time constant of a nerve is shortened under hyperglycemia, suggesting reduced axonal persistent Na+ currents. However, the time constant is also affected by changes in passive membrane properties. Latent addition using computerized threshold tracking is a new method that can separately evaluate Na+ currents and passive membrane properties. METHODS: Latent addition was used to estimate nodal Na+ currents in median motor axons of 83 diabetic patients. Brief hyperpolarizing conditioning current pulses were delivered, and threshold changes at the conditioning-test interval of 0.2 ms were measured as an indicator of nodal persistent Na+ currents. Seventeen patients were examined before and after insulin treatment. RESULTS: There was an inverse linear relationship between hemoglobin A1c levels and threshold changes at 0.2 ms (P=0.02); the higher hemoglobin A1c levels were associated with smaller threshold changes. After insulin treatment, there was a significant improvement in nerve conduction velocities associated with greater threshold changes at 0.2 ms (P=0.03), suggesting an increase in persistent Na+ currents. The fast component of latent addition, an indicator of passive membrane properties, was not affected by the state of glycemic control. CONCLUSIONS: Hyperglycemia could suppress nodal persistent Na+ currents, presumably because of reduced trans-axonal Na+ gradient or impaired Na+ channels, and this can be rapidly restored by glycemic control. SIGNIFICANCE: Reduced nodal Na+ currents may partly contribute to the pathophysiology of human diabetic neuropathy.

Action Potentials↗
PubMed2006

Altered axonal excitability properties in amyotrophic lateral sclerosis: impaired potassium channel function related to disease stage.

Fasciculations are a characteristic feature of amyotrophic lateral sclerosis (ALS), and can arise proximally or distally in the motor neuron, indicating a widespread disturbance in membrane excitability. Previous studies of axonal excitability properties (i.e. threshold electrotonus, strength-duration time constant) have suggested respectively that change in potassium or sodium channels may be involved. To reinvestigate these changes and explore their correlation with disease stage, multiple axonal excitability properties (threshold electrotonus, strength-duration time constant, recovery cycle and current-threshold relationship) were measured for the median nerve at the wrist in 58 ALS patients, and compared with 25 age-matched controls. In ALS, there were greater changes in depolarizing threshold electrotonus (i.e. less accommodation) (P < 0.001) and greater supernormality in the recovery cycles (P < 0.001). These abnormalities were more prominent in patients with moderately reduced CMAP (1-5 mV). Modelling the excitability changes in this group supported the hypothesis that axonal potassium conductances are reduced, resulting in increased supernormality despite membrane depolarization. The tendency for strength-duration time constant to be prolonged in ALS was only significant for patients with normal CMAP amplitude (>5 mV). Patients with severely reduced CMAP (<1 mV) alone showed reduced threshold changes to hyperpolarizing current. These results suggest a changing pattern of abnormal membrane properties with disease progression. First, persistent Na+ conductance increases, possibly associated with collateral sprouting, and then K(+) conductances decline. Both changes cause axonal hyperexcitability, and may contribute to the generation of fasciculations. These serial changes in axonal properties could provide insights into the pathophysiology of ALS, and implications for future therapeutic options.

Adult↗
PubMed2005

Dependence of platelet thrombus stability on sustained glycoprotein IIb/IIIa activation through adenosine 5'-diphosphate receptor stimulation and cyclic calcium signaling.

OBJECTIVES: We sought to evaluate the mechanisms that support the stability of platelet aggregates on a thrombogenic surface exposed to flowing blood. BACKGROUND: Activation of the membrane glycoprotein (GP) IIb/IIIa--mediated in part through the P2Y1 and P2Y12 adenosine 5'-diphosphate (ADP) receptors--is necessary for platelet aggregation. Platelets in growing thrombi exhibit cyclic calcium signal, suggesting that sustained activation may be required for thrombus stability. METHODS: Blood was perfused over type I collagen fibrils at the wall shear rate of 1,500 s(-1). Three-dimensional visualization of platelet thrombi was obtained in real time with confocal microscopy. The intracytoplasmic Ca2+ concentration ([Ca2+]i) was measured in fluo-3AM-loaded platelets. RESULTS: The height of platelet thrombi in control blood was 13.5 +/- 3.3 microm after 6 min, and increased to 16.3 +/- 4.5 microm (n = 8) after an additional 6 min. In contrast, the height was reduced to 5.4 +/- 2.2 and 3.3 +/- 1.3 microm, respectively (p < 0.01, n = 8), when the blood used in the second 6-min perfusion contained a P2Y1 (MRS2179) or P2Y12 (AR-C69931MX) inhibitor. The [Ca2+]i of platelets within forming thrombi oscillated between 212 +/- 38 nmol/l and 924 +/- 458 nmol/l, with cycles lasting 4.2 +/- 2.8 s that were inhibited completely by AR-C69931MX and partially by MRS2179. Accordingly, thrombi became unstable upon perfusion of blood containing the Ca2+ channel blocker, lanthanum chloride. Flow cytometric studies demonstrated that AR-C69931MX, MRS2179, and lanthanum chloride reduced monoclonal antibody PAC-1 binding to platelets, indicating a decrease of membrane-expressed activated GP IIb/IIIa. CONCLUSIONS: Continuous P2Y1 and P2Y12 stimulation resulting in cyclic [Ca2+]i oscillations is required for maintaining the activation of GP IIb/IIIa needed for thrombus stability in flowing blood.

Adenosine Monophosphate↗
PubMed2005

Concomitant chronic inflammatory demyelinating polyneuropathy and myasthenia gravis following cytomegalovirus infection.

We describe a patient who concomitantly developed chronic inflammatory demyelinating polyneuropathy (CIDP) and myasthenia gravis (MG) following cytomegalovirus (CMV) infection. Whereas CIDP and MG presumably have different immunopathogeneses, a number of reports presented cases with CIDP and MG, some of which were concomitant cases. Several reports described association between CIDP or MG, and CMV infection, although the association is still a matter of controversy. This is the first report of patients with concomitant CIDP and MG following CMV infection. The association may be coincidental, but the possibility that CMV infection triggered development of both CIDP and MG simultaneously cannot be excluded.

Cytomegalovirus Infections↗
PubMed2005

Activation of hepatic branched-chain alpha-keto acid dehydrogenase complex by tumor necrosis factor-alpha in rats.

Tumor necrosis factor-alpha (TNFalpha) promotes oxidation of branched-chain amino acids (BCAA). BCAA catabolism is regulated by branched-chain alpha-keto acid dehydrogenase (BCKDH) complex, which is regulated by phosphorylation-dephosphorylation of the E1alpha subunit at Ser293. BCKDH kinase is responsible for inactivation of the complex by phosphorylation. In the present study, we examined the effects of TNFalpha administration on hepatic BCKDH complex and kinase in rats. Rats were intravenously administered with 25 or 50 microg TNFalpha/kg body weight 4 h prior to sacrifice. The TNFalpha treatment at both doses elevated the activity state (percentage of the active form) of BCKDH complex from 22% to 69% and 86%, respectively, and the amount of phospho-Ser293 on the E1alpha subunit in each group of rats corresponded inversely to the activity state of BCKDH complex. The TNFalpha treatment of rats significantly decreased the activity as well as the bound form of BCKDH kinase. These results suggest that the decrease in the bound form of kinase is involved in the mechanism responsible for TNFalpha-induced activation of the BCKDH complex.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2005

The acute effects of glycemic control on nerve conduction in human diabetics.

OBJECTIVE: To investigate acute changes in nerve conduction associated with glycemic control. In diabetes, nerve dysfunction can result from reversible metabolic factors associated with hyperglycemia, as well as structural changes. METHODS: Multiple nerve conduction parameters including F-wave latencies were measured in 47 diabetic patients with prominent hyperglycemia before and after intensive insulin treatment. RESULTS: Four weeks after the start of treatment, there was a significant improvement in minimal F-wave latencies of the median (P<0.001) and tibial (P<0.001) nerves, and in distal latencies (P=0.01) and sensory nerve conduction velocities (P<0.001) of the median nerves. Amplitudes of motor and sensory responses did not change significantly. These findings were similar for patients with type 1 (n=8) and those with type 2 (n=39) diabetes. Patients with poorer glycemic control or milder neuropathy tended to show greater changes after treatment. CONCLUSIONS: Glycemic control quickly alters the speed of nerve conduction. F-wave latencies and conduction times across the carpal tunnel are very sensitive parameters. SIGNIFICANCE: Serial nerve conduction studies can detect reversible slowing of nerve conduction presumably caused by metabolic factors, such as decreased Na+/K+-ATPase activity, the altered polyol pathway, and tissue acidosis.

Action Potentials↗