Identification of a rat invariant T-cell receptor; alpha chain similar to mouse V alpha 14-J alpha 281 and human V alpha 24-J alpha Q.
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Amino Acid Sequence↗
Biomedical subjects
Y Hashimoto
Publications and source records attributed to Y Hashimoto.
Multiple lymphomatous polyposis of the gastrointestinal tract is a heterogenous group that includes mantle cell lymphoma and follicular lymphoma: analysis of somatic mutation of immunoglobulin heavy chain gene variable region.
Multiple lymphomatous polyposis (MLP) is characterized by multiple polyps involving long segments of the gastrointestinal (GI) tract. MLP is thought to represent mantle cell lymphoma (MCL) of the GI tract; however, some cases of follicular lymphoma (FL) of the GI tract are found with a multiple polypoid appearance. In the present study, to clarify the cellular origin of MLP, clonal immunoglobulin heavy chain (IgH) gene rearrangement of four cases with MLP was amplified by polymerase chain reaction (PCR) and analyzed for the presence of somatic mutation. The IgH variable (VH) region sequences of three cases (CD5+ CD10- cyclin D1+) showed a little somatic mutation compared with the closest published germline. The other case (CD10+ CD5- cyclin D1-) was highly mutated and showed intraclonal heterogeneity (ongoing somatic hypermutation). These data indicate that three of the cases with MLP are derived from pregerminal center B cells (mantle zone B cells) and one case with MLP from germinal center B cells. Our study suggests that MLP is a heterogenous group that includes MCL and FL.
Adult↗
Embolectomy for acute embolic occlusion of the internal carotid artery bifurcation.
BACKGROUND: Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. METHODS: We report the results of emergency embolectomy in six patients with acute embolic occlusion of the internal carotid artery (ICA) bifurcation. All six patients were admitted to our institute within 2 h of the onset of symptoms. Computed tomography (CT) scans on admission revealed no low-density or high-density regions in any patients. The time between onset of symptoms and completion of angiography ranged from 2 to 4 h (2.8 +/- 0.7 h). RESULTS: Emergency embolectomy was performed for each patient. Recanalization was confirmed angiographically in four of the patients. In the remaining two patients, massive infarction in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was not performed in these two cases. These two patients died of uncal herniation 6 days after onset. Two of the six patients were able to walk with a cane 2 months after surgery. The remaining two patients were unable to walk or attend to their own bodily needs without assistance. The time elapsed between onset of symptoms to reopening of the occluded vessel was within 6 h in the four surviving patients. The recanalization rate was 66.7% (4/6) for the embolectomy procedure, significantly higher than that (12.5%) of the thrombolytic therapy reported in a previous study. CONCLUSIONS: In summary, open embolectomy can be performed when the time after onset of symptoms is less than 6 h.
Acute Disease↗
Effects of ALCAR on the fast axoplasmic transport in cultured sensory neurons of streptozotocin-induced diabetic rats.
The effects of acetyl-L-carnitine (ALCAR) on fast axoplasmic transport were studied in cultured dorsal root ganglion (DRG) neurons of diabetic rats. Three-month-old male rats were used 7 days after streptozotocin injection. Neurons obtained from ganglia were cultured with a high concentration of glucose. The amount and the mean velocity of retrogradely transported particles, reduced in the diabetic animal, were transiently recovered by 1 mM ALCAR. The number of particles moving at 0.8-1.2 microm/s, considered to be lysosomes, increased in the velocity distribution. ALCAR did not modify the amount and mean velocity of anterograde particles which were unaffected by diabetes, or of bidirectional particles in neurons of control rats. This study suggests that diabetic neuropathy may be relieved by ALCAR via recovering retrograde axoplasmic transport.
Acetylcarnitine↗
Microtubule-associated protein-2 in the hypothalamo-neurohypophysial system: low-molecular-weight microtubule-associated protein-2 in pituitary astrocytes.
Microtubule-associated protein-2 is the most abundant microtubule-associated protein in the brain and is responsible for morphogenesis and maintenance of the nervous system. In the present experiments, we have examined the localization of microtubule-associated protein-2 in the hypothalamo-neurohypophysial system of the rat using western blots and immunohistochemistry. Two monoclonal antibodies against microtubule-associated protein-2, antibody C and AP20, were used: antibody C recognizes both the high- and low-molecular-weight isoforms of microtubule-associated protein-2; antibody AP20 specifically detects high-molecular-weight microtubule-associated protein-2 only. Western blot analysis revealed expression of high-molecular-weight microtubule-associated protein-2 in the whole brain, hippocampus and whole hypothalamus. While the supraoptic nucleus expressed only high-molecular-weight microtubule-associated protein-2, the adult posterior pituitary predominantly expressed low-molecular-weight microtubule-associated protein-2, which was also seen in the embryonic whole brain. Light microscopic immunohistochemistry revealed that both antibody C and AP20 intensely stained dendrites of the dendritic and somatic zones in the supraoptic nucleus. Double labeling with antibodies against microtubule-associated protein-2 and oxytocin (or vasopressin) demonstrated that microtubule-associated protein-2 was localized in dendrites of magnocellular neurons in the supraoptic nucleus. In the posterior pituitary, however, antibody C stained fine processes and cell bodies of astrocytes, which were identified by an antibody against glial fibrillary acidic protein. Antibody AP20 also stained fine processes of some astrocytes in the posterior pituitary, but the intensity of immunoreactivity with antibody AP20 was weaker than that with antibody C. This result suggests that microtubule-associated protein-2 in astrocytes of the posterior pituitary is predominantly of the low-molecular-weight type. Moreover, western blots revealed low-molecular-weight microtubule-associated protein-2 of the posterior pituitary at a molecular weight slightly higher than embryonically expressed low-molecular-weight microtubule-associated protein-2, indicating that low-molecular-weight microtubule-associated protein-2 in the posterior pituitary is possibly the isoform microtubule-associated protein-2d. The present results demonstrate that astrocytes in the posterior pituitary of adult rats still retain the ability to express the immature variant of microtubule-associated protein-2, low-molecular-weight microtubule-associated protein-2, and its expression is probably linked to structural plasticity.
Animals↗
Sudden recurrent laryngeal nerve paralysis due to apoplexy of parathyroid adenoma.
Neoplastic lesions of the parathyroid are rare, and most of these are adenomas. Even rarer is a secondary involvement of the recurrent laryngeal nerve. A case is presented of sudden onset hoarseness in a 64-year-old man caused by acute vocal cord paralysis due to bleeding within an adenoma of the lower right parathyroid gland. Acute onset of vocal cord paralysis is rarely associated with benign processes; the current case is only the second report associated with parathyroid adenoma.
Adenoma↗
Deformation of the acetabular polyethylene liner and the backside gap.
Polyethylene wear of acetabular components may cause osteolysis and aseptic loosening in total hip arthroplasty. Case reports of wear between the polyethylene liner and acetabular metal backing (backside wear) have promoted speculation on the clinical importance of debris generation at this site and the potential importance of insert conformity. We examined 90 retrieved nonconforming acetabular components from a single manufacturer. Twenty-four liners (27%) showed polyethylene deformation corresponding to screw holes on the backside surface. The location of screw-hole deformations corresponded to the direction of polyethylene deformation (wear) on the articular surface in all cases. The polyethylene liners with backside deformations were significantly thinner than the liners without deformation (P = .02). The presence of acetabular osteolysis did not significantly correlate with backside deformation, but there was a significant association between osteolysis and wear of the articular surface (P = .0004). In this implant design, backside deformation (wear) may not be due to micromotion at the interface but to the viscoelastic nature of ultra-high-molecular weight polyethylene.
Acetabulum↗
Effects of arbekacin and vancomycin on release of lactate dehydrogenase and fragmentation of DNA in LLC-PK1 kidney epithelial cells.
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Aminoglycosides↗
Distribution characteristics of levofloxacin and grepafloxacin in rat kidney.
PURPOSE: To elucidate the renal distribution of quinolones, we examined the uptake of levofloxacin and grepafloxacin in vivo and in rat renal cortical slices. METHODS: The plasma and various tissue concentrations of levofloxacin and grepafloxacin were measured after a bolus injection in rats, and tissue uptake clearance was calculated. Transport characteristics of quinolones in rat renal cortical slices were evaluated. RESULTS: The tissue distribution of levofloxacin and grepafloxacin in the kidney was greater than in any other tissue, and the tissue uptake clearances of levofloxacin and grepafloxacin in the kidney cortex were 1.2 and 4.6 ml/min/g tissue, respectively. The uptake of levofloxacin and grepafloxacin in rat renal cortical slices was concentrative, as indicated by slice/medium ratios of 2.3 and 9.6 at 60 min, respectively. The uptake of levofloxacin and grepafloxacin in rat renal cortical slices showed saturation, and was significantly inhibited in the presence of quinidine (p<.05), but not of tetraethylammonium or p-aminohippurate. CONCLUSIONS: Renal distribution of levofloxacin and grepafloxacin may be mediated by a specific transport system for quinolones, distinct from the organic cation and organic anion transport systems in the kidney.
Animals↗
Effects of glibenclamide on glycylsarcosine transport by the rat peptide transporters PEPT1 and PEPT2.
1 Glibenclamide is a widely used sulphonylurea for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). This agent has been reported to inhibit the activities of various ion channels and transporters. In the present study, we examined the effects of glibenclamide on the function of the H+/peptide cotransporters PEPT1 and PEPT2 by using stable transfectants. 2 Uptake of [14C]-glycylsarcosine, a typical substrate for peptide transporters, by PEPT1- or PEPT2-expressing transfectant was inhibited by glibenclamide as well as other sulphonylureas including tolbutamide. 3 Kinetic analysis revealed that the inhibition by glibenclamide was noncompetitive. Dixon plot analyses showed that the Ki values of this agent were 25 and 7.8 microM for PEPT1 and PEPT2, respectively. 4 Glibenclamide did not inhibit Na+-coupled alanine and alpha-methyl-D-glucoside transport, suggesting that the inhibitory effects of glibenclamide on peptide transporters were not due to nonspecific interactions. 5 There was little uptake of [3H]-glibenclamide by PEPT-expressing transfectants as compared to mock-transfected cells, suggesting that glibenclamide was not a substrate for these peptide transporters. 6 In summary, glibenclamide inhibited the [14C]-glycylsarcosine transport by PEPT1 and PEPT2 in a noncompetitive fashion, although glibenclamide per se was not transported through these transporters. These findings would provide important information for clinical, physiological and biochemical aspects of peptide transporters.
Alanine↗
The role of Ets family transcription factor PU.1 in hematopoietic cell differentiation, proliferation and apoptosis.
The PU.1 gene encodes an Ets family transcription factor which controls expression of many B cell- and macrophage-specific genes. Expression of the gene is critical for development of lymphoid and myeloid cell lineages, since PU.1-deficient mice exhibit defects in the development of these cell lineages. The PU.1 gene is identical to the Spi-1 gene isolated from common proviral integration sites in Friend virus-induced murine erythroleukemia (MEL), and deregulated expression of the gene is believed to be an essential step of the disease. We recently demonstrated that overexpression of PU.1 inhibits erythroid differentiation of MEL cells induced with the differentiating agent DMSO. We also noticed unexpectedly that overexpression of PU.1 together with DMSO induces marked growth arrest and apoptosis in MEL cells, supporting the notion that some oncogenes induce growth inhibition and apoptosis rather than cell proliferation and transformation under specific circumstances as shown with the c-myc gene. In this review, the role of PU.1 in hematopoietic cell differentiation, proliferation and apoptosis is described and the possible molecular mechanisms of PU.1-induced effects in MEL cells are discussed.
Animals↗
Programmed cell death in normal epidermis and loricrin keratoderma. Multiple functions of profilaggrin in keratinization.
The terminal differentiation of epidermal keratinocytes has been regarded as an example of programmed cell death. Among the proteins specifically expressed in this process is profilaggrin, which consists offilaggrin repeats and N- and C-terminal domains. Profilaggrin is proteolytically processed into individual domains during the terminal differentiation. Filaggrin released from profilaggrin aggregates keratin filaments to form compacted cornified cells with a keratin pattern. A recent transfection experiment has indicated initiation of cell death by filaggrin expression constructs. The transitional cells between the granular and cornified cells show morphologic characteristics of apoptotic cells, and their nuclei contain fragmented DNA and profilaggrin N-terminal domains. This suggests that the N-terminus of profilaggrin may participate in nuclear events accompanying programmed cell death. Among inherited skin disorders with abnormal keratinization, progressive symmetric erythrokeratoderma is caused by loricrin mutation (loricrin keratoderma). In this disease, profilaggrin N-terminal domains are aggregated with mutant loricrin within condensed nuclei. These nuclei persist in the cornified layer as parakeratosis. Loricrin keratoderma could therefore be regarded as a representative form of disrupted cell death.
Animals↗
Analysis of the immunoglobulin heavy chain gene variable region of 101 cases with peripheral B cell neoplasms and B cell chronic lymphocytic leukemia in the japanese population.
We have analyzed the immunoglobulin heavy chain (VH) gene variable regions (CDR2 and FW3) of 101 Japanese cases with peripheral B cell neoplasms. When all except one case with a deletion were graphed by frequency of replacement mutation, the 100 cases could be separated into two groups: 24 cases with zero, one and two mutations (germline or low frequency of somatic mutation); and 76 cases with three or more mutations (medium to high frequency of somatic mutation). While most mantle cell lymphoma cases (11/13) showed germline or low frequency of somatic mutation, all cases of mucosa-associated lymphoid tissue (MALT) lymphoma (11/11), follicular lymphoma (three of three cases), plasma cell myeloma (seven of seven cases) and most cases of diffuse large B cell lymphoma (DLBCL; 42/47) belonged to the latter group. These 76 cases, therefore, may be considered to show somatic hypermutation. More than half of chronic lymphocytic leukemia/small lymphocytic lymphoma cases (CLL/SLL; eight of 13) showed a hypermutated VH gene and the ratio of replacement mutation: silent mutation in CDR2 of CLL/SLL was considerably higher compared with DLBCL and MALT lymphoma, showing somatic hypermutation. When comparing VH gene type of B cell-CLL (B-CLL) among our series and those in the literature, more cases of CD5+ B-CLL in the Western literature have the VH5 and VH6 family types, while more cases in Japan are reported to have VH4 family. The occurrence of VH families in B-CLL between Japanese and Western people seems to be comparable.
Aged↗
Identification and characterization of a new intermediate in the ribosylative inactivation pathway of rifampin by Mycobacterium smegmatis.
Mycobacterium smegmatis DSM 43756 inactivates rifampin by ribosylation. To study this process of rifampicin, all possible inactivated forms of the antibiotic were extracted and purified. Structural studies showed the presence of a new inactivation product, designated RIP-TAp(23-phosphoribosyl-rifampin). Formation of 23-(O-ADP-ribosyl)rifampin (RIP-TAs) is the first step, followed by removal of AMP to give rise to the newly identified compound. Lastly, dephosphorylation leads to formation of 23-ribosyl-rifampin (RIP-Mb). Feeding experiments with the ADP-ribosylated antibiotic obtained from the cell homogenates of an Escherichia coli strain carrying the cloned M. smegmatis gene confirmed this rifampin inactivation process.
Antibiotics, Antitubercular↗
I.v. lidocaine worsens histamine-induced bronchoconstriction in dogs.
We have assessed the effect of lidocaine (lignocaine) on histamine-induced bronchoconstriction by direct visualization with a superfine fibreoptic bronchoscope. Seven mongrel dogs were anaesthetized with pentobarbital (pentobarbitone) 30 mg kg-1 followed by 2 mg kg-1 h-1 and pancuronium 200 micrograms kg-1 h-1. The trachea was intubated with a tracheal tube containing a second lumen for insertion of a 2.2-mm fibreoptic bronchoscope. This allowed estimation of the bronchial cross-sectional area (BCA) of the third bronchial bifurcation of the right lung. We used NIH image, a public domain image processing and analysis program. Bronchoconstriction was produced with a bolus dose of histamine 10 micrograms kg-1 i.v. followed by continuous infusion of 500 micrograms kg-1 h-1. After 30 min the following i.v. doses of lidocaine were given: lidocaine 0 (saline), 0.01, 0.1, 1.0 and 10 mg kg-1 at 10-min intervals. BCA was assessed 90 s after each dose. Arterial blood sampling was performed for measurement of plasma catecholamines. Lidocaine 1.0 and 10 mg kg-1 significantly reduced histamine-decreased BCA from 69.7 (SEM 4.1)% to 59.8 (7.3)% and 34.3 (6.8)%, respectively. Plasma concentrations of catecholamines decreased significantly after lidocaine 10 mg kg-1 i.v. In addition, there was a significant correlation between percentage decreases in plasma concentrations of epinephrine (adrenaline) and norepinephrine (noradrenaline) and reduction in %BCA (epinephrine-BCA, P < 0.01, r = 0.674; norepinephrine-BCA, P < 0.01, r = 0.510). This study suggests that i.v. lidocaine may exacerbate histamine-induced bronchoconstriction by a sympatholytic effect. This may have therapeutic implications for patients with acute asthma or anaphylactic shock who may become dependent on circulating catecholamines.
Anesthetics, Intravenous↗
Low-dose succinylcholine facilitates laryngeal mask airway insertion during thiopental anaesthesia.
We have assessed the optimal dose of succinylcholine to provide satisfactory conditions for insertion of a laryngeal mask airway (LMA) without causing myalgia during induction of anaesthesia with thiopental. We studied 60 adult patients, allocated randomly to one of three groups: group 1 (n = 20) received normal saline, group 2 (n = 20) received succinylcholine 0.25 mg kg-1 and group 3 (n = 20) received succinylcholine 0.5 mg kg-1. Insertion of the LMA was performed 1 min after administration of succinylcholine or saline. Insertion conditions were significantly better in group 3 compared with groups 1 and 2. The incidence of adverse responses on insertion was significantly higher in groups 1 and 2 than in group 3. Four of 20 patients (20%) in group 3 complained of myalgia, which was higher than that in group 1 (0%) and group 2 (10%), but there were no significant differences between groups on the day of operation. On day 3 after operation, seven patients (35%) in group 3 complained of myalgia, which was significantly higher than that in group 1 (5%) and group 2 (20%). Time from administration of succinylcholine to resumption of spontaneous respiration was significantly longer in groups 2 (194.9 (SD 50.4) s) and 3 (234.2 (34.3) s) than in group 1 (84.7 (32.4) s). There was also a significant difference between groups 3 and 2 for duration of apnoea.
Adult↗
Relaxant effect of propofol on the airway in dogs.
Propofol has been suggested to produce airway relaxant effects in vivo, although the mechanism is unclear. We have evaluated the bronchodilating effect of propofol using a direct visualization method with a superfine fibreoptic bronchoscope. We studied 21 mongrel dogs anaesthetized with pentobarbital 30 mg kg-1 i.v. and pancuronium 0.2 mg kg-1 h-1. The animals were allocated randomly to one of three groups (n = 7 in each): propofol group, atropine-propofol group and histamine-propofol group. The trachea was intubated using a tracheal tube that had a second lumen for insertion of the bronchoscope to monitor continuously bronchial cross-sectional area (BCA). BCA was measured using the NIH Image program. In the propofol group, dogs were given the following doses of propofol at 10-min intervals: 0 (saline), 0.2, 2.0 and 20 mg kg-1 i.v. In the atropine-propofol group, saline, atropine 0.2 mg kg-1 and propofol 20 mg kg-1 were given at 10-min intervals. In the histamine-propofol group, bronchoconstriction was elicited with histamine 10 micrograms kg-1 and 500 micrograms kg-1 h-1 until the end of the experiment. Thirty minutes after the start of infusion of histamine, propofol (0, 0.2, 2.0 and 20 mg kg-1) was administered. Changes in BCA were expressed as percentage of basal area. Histamine decreased BCA by 39.2 (SEM 5.4%). Propofol increased significantly basal and histamine-decreased BCA in a dose-dependent manner by 18.4 (4.5%) and 15.8 (4.9%), respectively after 20 mg kg-1 i.v. However, propofol following atropine i.v. did not increase BCA (129.9 (8.2)% after atropine vs 125.7 (8.9)% after propofol). Therefore, the relaxant effect of propofol may be a result of reduction in vagal tone.
Anesthetics, Intravenous↗
Isolation and characterization of a novel HS1 SH3 domain binding protein, HS1BP3.
We have isolated a novel gene, HS1BP3, which encodes an HS1 binding protein. Analysis of HS1BP3 cDNA indicates several potentially important segments, including a PX domain, a leucine zipper, immunoreceptor tyrosine-based inhibitory motif-like motifs and proline-rich regions. HS1BP3 associates with HS1 proteins in vivo as confirmed by immunoprecipitation in B and T cell lines. HS1BP3 preferentially associates with the HS1 SH3 domains rather than with other SH3 molecules, suggesting a role of HS1BP3 as an HS1 signaling mediator. Overexpression of mutant HS1BP3 protein in T cell lines results in decreased IL-2 production. Our data suggest a novel role for HS1BP3 in lymphocyte activation.
Adaptor Proteins, Signal Transducing↗