Search PubMed⌕ Search

Biomedical subjects

F Nakamura

Publications and source records attributed to F Nakamura.

At least 73 records · Page 4Linked to original sources
PubMed1999

Analysis of rapid eye movement periodicity in narcoleptics based on maximum entropy method.

We examined REM sleep periodicity in typical narcoleptics and patients who had shown signs of a narcoleptic tetrad without HLA-DRB1*1501/DQB1*0602 or DR2 antigens, using spectral analysis based on the maximum entropy method. The REM sleep period of typical narcoleptics showed two peaks, one at 70-90 min and one at 110-130 min at night, and a single peak at around 70-90 min during the daytime. The nocturnal REM sleep period of typical narcoleptics may be composed of several different periods, one of which corresponds to that of their daytime REM sleep.

Adult↗
PubMed1999

A comparison of post-ictal headache between patients with occipital lobe epilepsy and temporal lobe epilepsy.

We investigated post-ictal headaches (PIH) using a questionnaire to ascertain their characteristics and compare them among different types of epilepsy. The subjects consisted of 34 patients with occipital lobe epilepsy (OLE) and 75 patients with temporal lobe epilepsy (TLE). PIH occurred in 62% of OLE and 23% of TLE (P < 0.05). The quality of pain in PIH was 'steady' in 71% of OLE and 29% of TLE (P < 0.05) as opposed to 'pounding'. Other factors, such as frequency, severity, duration, and accompanying symptoms showed no significant differences. We found very few patients with migraine-like headaches. Analyses of clinical factors, such as age at onset, duration of epilepsy, seizure frequency, family history of headache, and interictal headache did not reveal any relationship to PIH, although generalized tonic-clonic seizures are associated with PIH in TLE (P < 0.05). These results suggest that the nature of PIH may be different between OLE and TLE, and that the region of epileptic focus or spreading area of epileptic discharge may have a close relation to the induction of PIH. An association with migraine, which has been reported previously, was unclear in our study.

Adult↗
PubMed1999

Regulation of F-actin binding to platelet moesin in vitro by both phosphorylation of threonine 558 and polyphosphatidylinositides.

Activation of human platelets with thrombin transiently increases phosphorylation at (558)threonine of moesin as determined with phosphorylation state-specific antibodies. This specific modification is completely inhibited by the kinase inhibitor staurosporine and maximally promoted by the phosphatase inhibitor calyculin A, making it possible to purify the two forms of moesin to homogeneity. Blot overlay assays with F-actin probes labeled with either [32P]ATP or 125I show that only phosphorylated moesin interacts with F-actin in total platelet lysates, in moesin antibody immunoprecipitates, and when purified. In the absence of detergents, both forms of the isolated protein are aggregated. Phosphorylated, purified moesin co-sediments with alpha- or beta/gamma-actin filaments in cationic, but not in anionic, nonionic, or amphoteric detergents. The interaction affinity is high (Kd, approximately 1.5 nM), and the maximal moesin:actin stoichiometry is 1:1. This interaction is also observed in platelets extracted with cationic but not with nonionic detergents. In 0.1% Triton X-100, F-actin interacts with phosphorylated moesin only in the presence of polyphosphatidylinositides. Thus, both polyphosphatidylinositides and phosphorylation can activate moesin's high-affinity F-actin binding site in vitro. Dual regulation by both mechanisms may be important for proper cellular control of moesin-mediated linkages between the actin cytoskeleton and the plasma membrane.

Actins↗
PubMed1999

A case of T-lineage lymphoblastic lymphoma/leukemia with t(4;11)(q21;p15) that switched to myelomonocytic leukemia at relapse.

A 51-year-old Japanese woman, initially diagnosed with T-lineage (CD2+, CD7+, CD3-, CD4-, CD8-) lymphoblastic lymphoma with t(4;11)(q21;p15), relapsed with acute myelomonocytic leukemia with the identical chromosomal abnormality. Southern-blot analysis revealed clonal rearrangements of an immunoglobulin heavy chain gene (JH) and T-cell receptor genes (J delta 1, J gamma 1, C beta 1) at first presentation, but germ line configurations of these genes at relapse. Leukemias with t(4;11)(q21;p15) may involve a hematopoietic progenitor capable of multilineage differentiation.

CD3 Complex↗
PubMed1998

Two distinct actin-binding sites of smooth muscle calponin.

Amino acid residues 145-163 of calponin have been proposed as a putative actin-binding site [Mezgueldi, M., Mendre, C., Calas, B., Kassab, R. & Fattoum, A. (1995) J. Biol. Chem. 270, 8867-8876]. Our previous work demonstrated that a fragment of calponin, which corresponded to the first repeated region of calponin and contained the preferred site of phosphorylation by protein kinase C [Nakamura, F., Mino, T., Yamamoto, J., Naka, M. & Tanaka, T. (1993) J. Biol. Chem. 268, 6194-6201] enhanced the Ca2+-induced contraction of permeabilized smooth muscle [Itoh, T., Suzuki, A., Watanabe, Y., Mino, T., Naka, M. & Tanaka, T. (1995) J. Biol. Chem. 270, 20400-20403]. In the present study, we compared the interactions with actin of a synthetic peptide (Lys172-His187) that encompassed the first repeated region with those of three other synthetic peptides. Lys172-His187 inhibited the binding of calponin to F-actin in a concentration-dependent manner but not the binding of caldesmon. Gly141-Gly160, including the above-mentioned putative actin-binding site, also competed with intact calponin to the same extent as Lys172-His187. Inhibition of actomyosin MgATPase activity was observed only with Gly141-Gly160. Lys172-His187 and other tested peptides had no effect. However, Gly141-Gly160 and Lys172-His187 reduced the fluorescence intensity of pyrene-labeled F-actin with approximately equal potency. Moreover, Lys172-His187 was able to reverse the inhibition of actomyosin MgATPase activity by calponin. Lys172-His187 was phosphorylated stoichiometrically by protein kinase C and phosphorylation of this peptide decreased its actin-binding activity. These observations suggest the direct involvement of two distinct actin-binding sites, with different regulatory functions, in the interactions of calponin with actin.

Actins↗
PubMed1998

Immunosuppressive and antiparasitic effects of cyclosporin A on Hymenolepis nana infection in mice.

The effect of cyclosporin A, which is known to act both as immunosuppressant and as an antiparasitic drug in many host-parasite systems, was examined in a mouse-Hymenolepis nana system. When BDF1 mice were injected s.c. with cyclosporin A (100 mg kg-1 day-1) every 48 h from 11 days p.i. with eggs, expulsion of the adult worms from the intestines of mice was prevented completely until at least 30 days p.i. Worm burden, dry weight and the number of gravid proglottids were not significantly reduced. By contrast, in untreated mice most of the worms were eliminated by 19 days p.i. The drug also completely abolished acquired resistance to a challenge infection with eggs when mice were injected s.c. with cyclosporin A (100 mg kg-1 day-1) around the time of challenge infection (Days -2, -1, 0, 1 and 2 relative to challenge). Such immunosuppressive effects of cyclosporin A on worm expulsion and protective immunity to reinfection were similar to those of another immunosuppressant, cyclophosphamide. As for the antiparasitic action of cyclosporin A against H. nana, a smaller number of cysticercoids developed from eggs in mice given cyclosporin A (100 mg kg-1 day-1) for 5 days beginning 1 day before infection, than in untreated controls.

Animals↗
PubMed1998

Translocation (10;12)(q24;q15) in a T-cell lymphoblastic lymphoma with myeloid hyperplasia.

We present a case of childhood T-cell lymphoblastic lymphoma (T-LBL) with a translocation (10;12)(q24;q15) as a main clonal abnormality, which to our knowledge is the first reported karyotype of this malignancy. The patient's peripheral blood and bone marrow showed marked leukocytosis mostly myeloid lineage cells, at diagnosis. The enlarged lymph node consisted of two different cell populations: CD2+/CD7+ prothymic lymphoblasts and a cluster of peroxidase-positive myeloid cells around vessels. This case might represent a rare but distinct clinical entity of LBL.

Adolescent↗
PubMed1998

Neuropilin-1 extracellular domains mediate semaphorin D/III-induced growth cone collapse.

Somatosensory axon outgrowth is repulsed when soluble semaphorin D (semD) binds to growth cone neuropilin-1 (Npn-1). Here, semD ligand binding studies of Npn-1 mutants demonstrate that the sema domain binds to the amino-terminal quarter, or complement-binding (CUB) domain, of Npn-1. By herpes simplex virus- (HSV-) mediated expression of Npn-1 mutants in chick retinal ganglion cells, we show that semD-induced growth cone collapse requires two segments of the ectodomain of Npn-1, the CUB domain and the juxtamembrane portion, or MAM (meprin, A5, mu) domain. In contrast, the transmembrane segment and cytoplasmic tail of Npn-1 are not required for biologic activity. These data imply that the CUB and MAM ectodomains of Npn-1 interact with another transmembrane growth cone protein that in turn transduces a semD signal into axon repulsion.

Animals↗
PubMed1998

Semaphorins A and E act as antagonists of neuropilin-1 and agonists of neuropilin-2 receptors.

Neuropilin-1 (NP-1) has been identified as a necessary component of a semaphorin D (SemD) receptor that repulses dorsal root ganglion (DRG) axons during development. SemA and SemE are related to SemD and bind to NP-1, but do not repulse DRG axons. By expressing NP-1 in retinal neurons and NP-2 in DRG neurons, we demonstrate that neuropilins are sufficient to determine the functional specificity of semaphorin responsiveness. SemA and SemE block SemD binding to NP-1 and abolish SemD repulsion in axons expressing NP-1. SemA and SemE seem to have a newly discovered protein antagonist capacity at NP-1 receptors, whereas they act as agonists at receptors containing NP-2.

Animals↗
PubMed1998

GAP-43 augmentation of G protein-mediated signal transduction is regulated by both phosphorylation and palmitoylation.

The neuronal protein GAP-43 is concentrated at the growth cone membrane, where it is thought to amplify the signal transduction process. As a model for its neuronal effects, GAP-43 protein injection into Xenopus laevis oocytes strongly augments the calcium-sensitive chloride current evoked by the G protein-coupled receptor stimulation. We have now examined a series of GAP-43 mutants in this system and determined those regions of GAP-43 required for this increase in current flux. As expected, palmitoylation inhibits signal amplification in oocytes by blocking G protein activation. Unexpectedly, a second domain of GAP-43 (residues 35-50) containing a protein kinase C phosphorylation site at residue 41 is also necessary for augmentation of G protein-coupled signals in oocytes. This region is not required for activation of isolated Go but is necessary for GAP-43 binding to isolated calmodulin and to isolated protein kinase C. Substitution of Asp for Ser41 inactivates GAP-43 as a signal facilitator in oocytes. This mutation blocks GAP-43 binding to both protein kinase C and calmodulin. Thus, GAP-43 regulates an oocyte signaling cascade via coordinated, simultaneous G protein activation and interaction with either calmodulin or protein kinase C.

Amino Acid Substitution↗
PubMed1998

Case report: Haemangioma of the small intestine complicated by protein-losing gastroenteropathy.

We report a case of haemangioma of the small intestine complicated by protein-losing gastroenteropathy. A 32-year-old female had suffered from hypoproteinaemia for 6 years, but the cause of this condition had not been determined. On diagnosis and therapy for hypoproteinaemia, intra-operative endoscopy and histological examination were performed and she was subsequently diagnosed with capillary haemangioma of the small intestine. Angiography was not useful for the detection of capillary haemangioma of the small intestine in this case. Although intestinal haemangioma is an important cause of gastrointestinal bleeding, protein loss is an extremely rare complication and this case is the first to be reported in Japan.

Adult↗
PubMed1998

Transcranial Doppler pattern after intracarotid papaverine and prostaglandin E1 incorporated in lipid microsphere in patients with vasospasm.

We studied the effects of intracarotid papaverine and prostaglandin E1 incorporated in lipid microsphere (Lipo-PGE1) in relation with transcranial Doppler parameters such as mean flow velocity (MFV) and pulsatile index (PI) of the proximal segment of the middle cerebral artery. Eighty patients with subarachnoid hemorrhage (SAH) were included in this study. In the case of angiographic vasospasm, papaverine at 7 mg/min with total dose below 300 mg per artery and 10-20 micrograms of Lipo-PGE1 were injected in the supraclinoid portion of the internal carotid artery. Vasospasm was improved in 24 patients (63%), however, it was unchanged in 14 patients (37%). The former patients had more favorable outcomes than the latter patients (p < 0.005). After intracarotid injection therapy, the correlation between MFV and PI was classified into three types: type 1, both MFV and PI decreased; type 2, MFV decreased but PI increased; and type 3, both MFV and PI fluctuated. The Glasgow Outcome Scale 3 months after SAH was as follows: type 1 (n = 15), good in 14 (93%) and moderate disability in one (7%); type 2 (n = 9), good in eight (89%) and vegetative state in one (11%); and type 3 (n = 14), moderate disability in five (36%), severe disability in seven (50%), and death in two (14%). Chi-square analysis showed significant differences between type 1 and type 3 (p < 0.005), and type 2 and type 3 (p < 0.005). In conclusion, intracarotid papaverine combined with Lipo-PGE1 was effective for vasospasm but type 3 patients require a different treatment protocol.

Alprostadil↗
PubMed1998

Measuring the diameter of coronary arteries on MR angiograms using spatial profile curves.

OBJECTIVE: The spatial profile curve of the nuclear MR intensity across the short axis of a coronary artery in an MR angiogram results in a gradual up-and-down slope lacking sharp definition, which indicates that display parameters may influence edge recognition. Therefore, our study was designed to determine the appropriate window setting and to devise a method of accurately measuring the diameter or width of the artery independent of window parameters. CONCLUSION: The diameter of a coronary artery measured on MR coronary arteriography significantly varied with experimentally selected display parameters. When compared with the diameter on contrast-enhanced coronary arteriograms, the window center on MR angiograms at the midpoint between the peak intensity of the intravascular lumen and the background intensity and the window width of a quarter or a half of the intensity difference between the two were proven to be appropriate. The angiographic diameter corresponded to the diameter obtained at 65% +/- 9% of the peak intensity on the spatial profile curve across the short-axis MR coronary angiogram. Accordingly, 65% of the peak intensity indicates the diameter of the coronary artery. Thus, the intensity profile curve independent of the window setting provided a new method for measurement of the diameter of the coronary artery.

Adult↗
PubMed1998

Vector analysis of the hemodynamics of atherogenesis in the human thoracic aorta using MR velocity mapping.

OBJECTIVE: Our study was designed to assess the applicability of MR velocity mapping for vector analysis of the hemodynamics of atherogenesis. SUBJECTS AND METHODS: MR velocity mapping was used to measure axial and nonaxial elements and the length of the wall shear rate (a spatial gradient of near-wall flow velocity parallel to the vessel wall) vector at 16 time points per cardiac cycle at eight anatomic locations of the thoracic aorta in six healthy subjects. An oscillatory shear index (a ratio of blood flow volume in the recessive direction divided by the sum of blood flow volume in both dominant and recessive directions) was introduced for analysis of the degree of oscillation. RESULTS: The time-averaged length, axial element, and nonaxial element of the wall shear rate vector were 118+/-53 sec(-1), 106+/-55 sec(-1), and 33+/-23 sec(-1), respectively. The oscillatory shear index in the axial direction was 0.06+/-0.10 and that in the nonaxial direction was 0.07+/-0.13. At the inner wall of the distal portion of the aortic arch, the length of the wall shear rate was smallest (74+/-32 sec(-1)) and oscillation in the axial direction was largest (0.16+/-0.19). CONCLUSION: Vector analysis of the wall shear rate in the thoracic aorta was successfully done with MR velocity mapping in humans. MR velocity mapping can noninvasively evaluate the hemodynamics of atherogenesis induced by the complicated blood flow.

Adult↗
PubMed1998

[A case of renal arteriovenous fistula diagnosed by pharmacoangiography].

A 17-year-old man, who had previously been followed for Nutcracker phenomenon, presented with back pain and gross hematuria. As he developed tamponade of the urinary bladder repeatedly, and the hemoglobin level decreased, we thus performed emergency angiography. A selective left renal venogram revealed the left renal vein to be compressed between the superior mesenteric artery and the abdominal aorta, while the development of an extensive peri- and para-renal collateral circulation was also observed. We next performed epinephrine pharmacoangiography in order to better visualize any abnormal vessels. A left renal arteriovenous fistula was thus diagnosed by this method, and treated successfully by transcatheter embolization using a platinum coil.

Adolescent↗
PubMed1997

Neuronal and non-neuronal collapsin-1 binding sites in developing chick are distinct from other semaphorin binding sites.

The collapsin and semaphorin family of extracellular proteins contributes to axonal path finding by repulsing axons and collapsing growth cones. To explore the mechanism of collapsin-1 action, we expressed and purified a truncated collapsin-1-alkaline phosphatase fusion protein (CAP-4). This protein retains biological activity as a DRG growth cone collapsing agent and saturably binds to DRG neurons with low nanomolar affinity. Specific CAP-4 binding sites are present on DRG neurons, sympathetic neurons, and motoneurons, but not on retinal, cortical, or brainstem neurons. Outside the nervous system, high levels of CAP-4 binding sites are present in the mesenchyme surrounding major blood vessels and developing bone and in lung. These sites provide a substrate for the collapsin-1-dependent patterning of non-neuronal tissues perturbed in sema III (-/-) mice. The staining patterns for mouse semaphorin D/III and chick collapsin-1 fusion proteins are indistinguishable from one another but quite separate from that for semaphorin B and M-semaphorin F fusion proteins. These data imply that a family of high-affinity semaphorin binding sites similar in complexity to the semaphorin ligand family exists.

Animals↗