Computation of the heavy-light decay constant using nonrelativistic lattice QCD.
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Journal Article↗
Biomedical subjects
S Hashimoto
Publications and source records attributed to S Hashimoto.
A potential role for antigen selection in the clonal evolution of Burkitt's lymphoma.
Burkitt's lymphoma (BL) is a monoclonal lymphoproliferative disorder characterized by the presence of specific chromosomal translocations that involve the c-myc proto-oncogene. Two subtypes of BL exist (endemic and sporadic) that differ in the prevalence of EBV genome expression. Although EBV infection may promote cellular proliferation in endemic BL, little is known about the forces that drive clonal expansion and evolution in the majority of EBV-negative sporadic BL. This study on an EBV-negative sporadic BL cell line derived from an AIDS patient provides evidence that antigenic stimulation may play a role in the development and/or expansion of such tumors. This cell line (BRG-P) contained a series of cellular clones that elaborated both IgM and IgA. Southern blot analyses of the line and its sublines indicated that both the IgM+ and IgA+ cells had identical c-myc and Ig JH gene rearrangements, indicating that they were derived from a common precursor, some of which eventually underwent an isotype switch. Ig VH gene sequence analyses of 21 molecular clones derived from the parental BRG BL line and two of its sublines demonstrated that all the clones used the same VH3 gene. Five unique intraclonal variants were identified at four distinct nucleotide positions (125, 161, 355, 375), which undoubtedly represented somatic mutations. Four of these five mutations occurred within complementary determining regions; all resulted in amino acid replacements. Moreover, an identical G to A nucleotide substitution that resulted in an identical amino acid change occurred at two distinct points in clonal evolution that were separated by the isotype class switch. Thus, the locations and types of the VH gene mutations, together with the occurrence of an isotype switch, are highly suggestive of an ongoing role for Ag stimulation and selection in the evolution of the malignant clone.
Adult↗
[The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension].
The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension (EH) was explored. After the measurement of blood pressure in 15 EH patients and 8 control subjects, EH patients were divided into two groups by the elevation of plasma NE (delta NE) 5 min after standing: 7 normoadrenergic EH (delta NE < 140 pg/ml) and 8 hyperadrenergic EH (delta NE > or = 140 pg/ml). On the morning after a 12-h overnight fast, regular insulin (0.1 U/kg) was injected intravenously, and glucose disappearance rate (GDR) was measured and used as an index of insulin sensitivity. On the following day, the test was reinvestigated following the administration of mabuterol, a beta 2 agonist. Plasma growth hormone (GH), cortisol, norepinephrine (NE) and epinephrine (Epi) were measured before and after the mabuterol administration. Although there were no significant differences of basal GDR among these three groups, mabuterol induced a considerable decrease in GDR in EH patients but not in control subjects. There was no significant difference in the decrease of GDR between normo- and hyperadrenergic EH. The decrease in GDR tended to correlate with the mean blood pressure at rest in EH but not in normal subjects. Plasma glucose and serum insulin in EH patients were increased more than in normal subjects. Plasma GH, cortisol and Epi were not elevated by mabuterol, but plasma NE increased in each group, significantly in hyperadrenergic EH. There was no correlationship between the increase in plasma NE and the decrease in GDR after mabuterol.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Agonists↗
Effects of activation-defective TBP mutations on transcription initiation in yeast.
Transcription initiation by RNA polymerase II is effected by an ordered series of general factor interactions with core promoter elements (leading to basal activity) and further regulated by gene-specific factors acting from distal elements. Both the general factor TFIID (refs 2,3), including the constituent TBP (TATA-binding polypeptide) and associated factors, and the interacting factor TFIIB (refs 9-11) have been implicated as targets for various activators. Towards an understanding of the basis for activator function, including the multiplicity of TBP interactions, we have now identified mutations in yeast TBP that selectively block activator (GAL4-VP16)-dependent but not basal transcription. We further show an effect of GAL4-VP16 on TFIIB recruitment to early preinitiation complexes, and that recruitment is disrupted by TBP mutations that impair its interactions with VP16 (L114K), TFIIB (L189K) or an unidentified component (K211L). Thus, GAL4-VP16 function seems to involve both direct interactions with TBP and a corresponding induction (or stabilization) of an activation-specific TBP-TFIIB-promoter complex.
Arabidopsis↗
[3H]SNF8702 autoradiography of CCK-B receptors in guinea pig brain and studies with a cloned rat CCK-B receptor.
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Animals↗
[Evaluation of surviving fraction using non-clonogenic staining densitometry method].
This study was performed to compare our nonclonogenic survival assay (densitometry assay, DM assay) with the widely used clonogenic assay. The established cell lines (HeLa, RMUG, IMR, GOTO) were grown in F 10 medium. The cells were spread in 24-well plates, irradiated with different doses, cultured for about one week and stained with crystal violet after the culture period. Taking the transparent images of the stained well on the light source with the CCD camera, the images were collected with the matrix size 64 x 64, and the integrated optical density of the entire surface of each well was determined by computer with our original program. As the number of cells in the well is reflected by its staining density, the surviving fraction was calculated as the fraction of growth in the irradiated wells relative to controls. The survival curves obtained by the densitometry method showed good correlations with those obtained by clonogenic assay. It is possible to predict intrinsic radiosensitivity with this assay, even if the cells do not form good colonies. However, this method is based on measurements in cultures which depend on the metabolism and growth kinetics of the irradiated cells. Cells should grow exponentially in the same manner in any well to obtain a result similar to that of clonogenic assay, although growth kinetics may be altered by irradiation. Thus, the endpoint must be strictly standardized.
Cell Survival↗
Parkinsonism induced by solvent abuse.
We report the first description of a patient with parkinsonism induced by solvent abuse. Our patient developed parkinsonism acutely, following heavy abuse of lacquer thinner. Her clinical deficits were indistinguishable from idiopathic parkinsonism (Parkinson's disease) and she responded to levodopa. Parkinsonism has persisted for more than 3 months. Brain computed tomography was normal. Positron emission tomographic studies showed normal fluorodopa uptake and reduced raclopride binding, indicating an unusual disturbance of striatal dopaminergic function. This patient suggests that organic solvents may cause parkinsonism in susceptible individuals.
Administration, Inhalation↗
Is facial nerve decompression surgery effective?
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Decompression, Surgical↗
Steroid therapy for facial nerve palsy in children.
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Adolescent↗
Experimental quantitative evaluation of transvascular removal of unnecessary substances in brain edema fluid.
We developed a model by which the transvascular removal of unnecessary substances in brain edema fluid could be measured quantitatively and chronologically. Brain stab wounds were produced in Wistar rats by insertion of paired microdialysis probes in the unilateral caudatoputamen. Homovanillic acid (HVA) was administered by microdialysis from one probe, and the HVA clearance was measured by HPLC analysis of perfusate from the other probe. Using this model, we evaluated the site of removal and whether the removal processes were affected by anesthesia or an elevated plasma concentration of the substance. As a result, 1) Probenecid did not change HVA clearance although this inhibits HVA removal via subarachnoid vessels. Therefore, HVA removal in this model was considered mainly due to intraparenchymal transvascular efflux. 2) There was no alteration in HVA removal induced by anesthesia or intravenous HVA injection. Consequently, this efflux mechanism seems to be a rather stable protective process, and seems to play a considerable role in brain microenvironmental homeostasis.
Animals↗
The complete sequence of the human CD79b (Ig beta/B29) gene: identification of a conserved exon/intron organization, immunoglobulin-like regulatory regions, and allelic polymorphism.
We determined the complete genomic sequence of the human CD79b (Ig beta/B29) gene. The CD79b gene product is associated with the membrane immunoglobulin signaling complex which is composed of immunoglobulin (Ig) itself, associated in a noncovalent fashion with CD79b and a second polypeptide chain, CD79a (Ig alpha/mb1). The sequence and exon/intron organization of the human and mouse CD79b genes are highly similar. The gene organization suggests that some variant forms of CD79b may arise by virtue of alternative splicing of mRNA. In addition, a number of conserved regulatory sequences commonly found in Ig genes are present in sequences which flank the human CD79b gene. Some of these sequences are distinct from those found in the CD79a promoter. These differences may explain why transcription of CD79b, but not CD79a, is observed in plasma cells. A new Taq 1 restriction fragment length polymorphism is described that is not associated with any structural polymorphisms of the expressed CD79b polypeptide.
Alleles↗
Chromosomal localization, genomic structure, and allelic polymorphism of the human CD79 alpha (Ig-alpha/mb-1) gene.
The germline DNA sequence of the human CD79 alpha (Ig-alpha/mb-1) gene was determined by polymerase chain reaction sequencing of a cosmid clone derived from an arrayed human chromosome 19 library. The CD79 alpha gene was localized to chromosome 19q13.2; this localization places the gene within the CEA-like gene cluster with the following gene order: -CEA-CGM1-CD79 alpha-RPS11-ATP1A3-BGP-CGM9-. The genomic organization of the human CD79 alpha gene resembles the mouse counterpart with five exons interrupted by four introns. Computer analyses suggest the presence of transcription regulatory elements known to be important in the regulation of mouse CD79 alpha (AP-1, EBF, AP-2, MUF2, and SP-1 sites), as well as elements not found in the mouse gene (an NK-kappa B binding site and a series of E-box motifs). Similar to the mouse gene, the 5' flanking region of human CD79 alpha lacks a TATA box; however, unlike mouse CD79 alpha, a classical octamer motif could not be identified in the human gene. Finally, a new Rsa I restriction fragment length polymorphism was defined in the non-coding regions of the human gene.
Amino Acid Sequence↗
Right atrial pressure and forearm blood flow during prolonged exercise in a hot environment.
Right atrial pressure (RAP) at rest is known to be reduced by an increase in skin blood flow (SkBF) in a hot environment. However, there is no clear evidence that this is so during exercise. To clarify the effect of the increase in SkBF on RAP during exercise, we measured forearm blood flow (FBF) (as an index of SkBF) and RAP continuously using a Swan-Ganz catheter in five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min in a hot environment (30 degrees C, relative humidity 20%). Cardiac output increased from 5.5 +/- 0.2 l/min at rest to 17.9 +/- 1.2 l/min (mean +/- SE, P < 0.01) in the first 10 min of exercise and then remained steady until the end of exercise. FBF did not change significantly during the first 5 min, but then increased from 2.7 +/- 0.5 ml/100 ml per min at rest to 10.8 +/- 1.7 ml/100 ml per min (P < 0.001) by 25 min as pulmonary arterial blood temperature (Tb) rose from 37.0 +/- 0.1 degrees C to 38.1 +/- 0.1 degrees C (P < 0.001). FBF then reached a plateau, despite a continuing increase in Tb. RAP increased significantly from 4.3 +/- 0.8 to 7.6 +/- 1.2 mm Hg (P < 0.001) during the first 5 min of exercise and then gradually declined to 6.1 +/- 1.0 mm Hg by 25 min (P < 0.001 vs. 5 min) and further to 5.7 +/- 1.0 mm Hg by 50 min, a value not significantly higher than at rest.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Involvement of clathrin light chains in the pathology of Alzheimer's disease.
Clathrin, which constitutes coated vesicles, plays important roles in neuronal functions. In the brains of the patients with Alzheimer's disease, distribution of clathrin was immunohistochemically investigated using four monoclonal antibodies against clathrin light chains, LCB.1, LCB.2, X-16 and CON.1, to study the involvement of clathrin in the pathology of Alzheimer's disease. LCB.1, LCB.2, X-16, and CON.1 bind to the aminoterminus of the clathrin light chain b(LCb), to the neuron-specific insert of LCb, to the light chain a(LCa), and to LCa and LCb, respectively. In Alzheimer brains, granular staining of LCB.2 around neurons in the hippocampus was weaker or patchily defected in comparison with control brains. Some neurofibrillary tangles and neurons were intensely stained in Alzheimer brains by LCB.2, whereas neurons were weakly stained in control brains. Crowns of some senile plaques in the brains of early onset Alzheimer's disease were positively stained by LCB.2. LCB.1 supported the observations of LCB.2. Reactive astrocytes in Alzheimer brains were intensely stained by X-16. On the other hand, Western blot analysis using LCB.2 and X-16 demonstrated no apparent differences in protein amounts and molecular weights of LCa and LCb between control and Alzheimer brains. These observations demonstrated abnormal distribution of clathrin in Alzheimer brains, implying impairment of axonal transport in this disease.
Adult↗
Effects of peritoneal insufflation on hepatic and renal blood flow.
The effects of peritoneal insufflation with carbon dioxide on hepatic and renal blood flow have not been reported hitherto. We evaluated these effects in a porcine model of abdominal laparoscopic surgery. Seven anesthetized pigs underwent peritoneal insufflation in a step-wise manner to create intraabdominal pressures of 6, 12, 18 and 24 mmHg, and changes in the arterial and venous pressure, arterial blood gases, and hepatic and renal blood flow were monitored. Both the hepatic and renal blood flow decreased as the intraabdominal pressure increased. Therefore, in order to carry out laparoscopic abdominal surgery safely in patients with hepatic or renal impairment, low intraabdominal pressures or noninsufflating techniques are recommended.
Animals↗
Effects of hepatic arterial infusion chemotherapy on unresectable or recurrent hepatocellular carcinoma.
We performed hepatic arterial infusion chemotherapy (HAI) on 86 patients with unresectable hepatocellular carcinoma (HCC, 61 patients) or unresectable recurrent HCC after hepatectomy (25 patients). As drug therapy, 250 mg of 5-fluorouracil was injected daily for 14 days using a reservoir embedded in the subcutaneous layer. During this period, 0.4 mg/kg of doxorubicin and 0.12 mg/kg of mitomycin C suspended in Lipiodol Ultra-Fluide were also injected twice intra-arterially. This was defined as one course of HAI, and it was repeated every 3 months. In the patients with unresectable HCC, the 1-, 2-, and 3-year survival rates were 31.5%, 22.4%, and 10.7%, respectively, and the numbers of cases showing a complete response (CR), a partial response (PR), a minor response (MR), no change (NC), and progressive disease (PD) according to the Criteria for the Evaluation of the Clinical Effects of Solid Cancer Chemotherapy established by the Japan Society for Cancer Therapy were 1 (1.6%), 20 (32.8%), 5 (8.2%), 28 (45.9%), and 7 (11.5%), respectively. On the other hand, the 1-, 2-, and 3-year survival rates of the patients with unresectable recurrent HCC were 69.6%, 34.8%, and 14.9%, respectively. The rate of catheter patency after 1 year was 64.1%, and the mean catheter-patency period was 311.9 days. Patients in group A (CR+PR, n = 21) survived significantly longer than those in group B (MR+NC+PD, n = 40; P < 0.05). In conclusion, since responders to HAI achieve longer survival than nonresponders, the selection of effective drugs is important for this therapy.
Adult↗
Unusual splice sites in the E1A-E1B cotranscripts synthesized in adenovirus type 40-infected A549 cells.
The adenovirus E1 DNA region consists of two transcription units, E1A and E1B. In this paper we report that the E1A-E1B cotranscripts containing sequences of both the E1A and E1B regions are synthesized during adenovirus type 40 (Ad40) infection of A549 cells. Cytoplasmic RNA was isolated from Ad40-infected A549 cells at 24, 72, and 100 h post infection (p.i.). The complementary (c) DNA was synthesized by reverse transcription using an oligo-dT primer and then amplified by the polymerase chain reaction (PCR) using primers derived from the E1A and E1B regions. The cDNAs thus amplified were sequenced either directly or after cloning into bacteriophage M13 vectors. Analysis of cDNA indicated that the E1A-E1B cotranscripts are synthesized at 72 h p.i., but not at 24 or 100 h p.i. Nucleotide sequences of three cDNAs of the E1A-E1B cotranscripts indicated that the cotranscripts originate from the E1A promoter and lack sequences for both the E1A poly(A) site and E1B cap site. The splices create open reading frames for E1A-E1B fused polypeptides around the E1A-E1B junctions in these mRNAs. Most interestingly, the sequence analysis showed that the 5' and 3' splice junctions in the two E1A-E1B cotranscripts do not conform to the splice consensus GT-AG rule. Our results thus suggest that factor(s) which lead to unusual splicing in the E1 mRNAs are present in Ad40-infected A549 cells.
Adenovirus E1A Proteins↗
Waveform changes of compound muscle action potential (CMAP) with muscle length.
Changes in finger positions influence the waveform of CMAP recorded from the muscle that moves that finger. The present study suggested that the muscle length, dependent on the finger position, was a main factor affecting the waveform. On shortening the muscle length, the amplitude of CMAP increased with concomitant reduction in the duration, and on lengthening, the amplitude decreased with concomitant increase in the duration. These changes are considered due to changes in propagation velocities of muscle fibers dependent on the muscle length. In nerve conduction studies, it is important to carefully monitor the finger position to distinguish the waveform changes with muscle length from those due to nerve lesions.
Action Potentials↗