Biomedical subjects

T Nishimura

Publications and source records attributed to T Nishimura.

At least 469 records · Page 26Linked to original sources

PubMed1996

Blink reflex in meningomyelocele, with special reference to its usefulness in the evaluation of brainstem dysfunction.

The electrically elicited blink reflex (BR) was studied in 30 patients with meningomyelocele (MMC), including 21 with Chiari type II malformation. The relationship between the BR and brainstem auditory evoked potentials (BAEPs) is discussed with regard to its usefulness in the evaluation of MMC's brainstem dysfunction. The following results were obtained: (1) The R2 component was abnormal in 90% of these patients. The BR disclosed subclinical lesions in the medulla oblongata which were not detected by BAEPs alone. (2) In all patients in whom the BAEPs suggested the presence of stretched cochlear nerves, the BR indicated the existence of some dysfunction of the medulla oblongata. (3) No close relationship was found between the dysfunction detected by the BR and the degree of hindbrain anomaly on the neuroimaging. (4) Combining results from assessment of the measurement of the BR and BAEPs permits evaluation of the function of the fifth, seventh, and eighth cranial nerves, as well as the brainstem including the medulla oblongata, which is more comprehensive than evaluation by neuroimaging alone.

Adolescent↗

PubMed1996

Somatosensory evoked potentials to median nerve stimulation in meningomyelocele: what is occurring in the hindbrain and its connections during growth?

Twenty patients with meningomyelocele (MMC) and shunted hydrocephalus, ranging in age from 3 to 23 years old, underwent serial recording of short-latency somatosensory evoked potentials (SEPs) to median nerve stimulation, on the basis of which to assess the evolution of dysfunction in the brainstem and its connections (cervical spinal cord, cervical nerve roots, lower cranial nerves). Eighteen patients had Chiari type II malformations, none of which was symptomatic. In all 20 patients, serial SEP recordings were obtained repeatedly after periods ranging from 2 to 7 years. The results were as follows: (1) the ratio of EP-N13 interpeak latencies (IPLs) to body height (BH) tended to lengthen gradually after starting in the normal range with growth. (2) In contrast, the ratio N13-N20 IPLs/BH decreased continuously to the normal range with growth, after initial prolongation. These findings and our earlier studies of brainstem auditory evoked potentials suggest that compression and traction result in strangulation of the cervical spinal cord and kinked medulla as well as stretching of the cervical nerve roots and lower cranial nerves. However, primary intrinsic functional disorders of the brainstem appeared to improve gradually during growth. The natural history of Chiari type II malformations involves these opposing dynamic phenomena in the hindbrain and its connections.

Adolescent↗

PubMed1996

Kinetics of radioiodinated species in subcellular fractions from rat hearts following administration of iodine-123-labelled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (123I-BMIPP).

It is recognized that iodine-123-labelled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (123I-BMIPP) slowly washes out of the myocardium. The mechanism for the washout was investigated in normal rat hearts by analyses of the subcellular distribution and lipid classes based on the BMIPP metabolism. Rat hearts were excised at 1-120 min after intravenous injection of 123I-BMIPP. After counting the radioactivity, the hearts were digested with Nagarse and homogenized, and then fractionated into the cytosolic, mitochondrial, microsomal and crude nuclear fractions by centrifugations. The radioactivity of each fraction was counted, and the lipid classes were analysed by radio-thin-layer chromatographic and high-performance liquid chromatographic methods. The heart uptake of 123I-BMIPP was maximal at 5 min (6.81%+/-0.36% ID/g), and 41% of the radioactivity disappeared within 120 min. The myocardial radioactivity was immediately distributed into the cytosolic, mitochondrial, microsomal and crude nuclear fractions. The distribution (%) of each fraction was almost identical from 5 min through 120 min. The cytosolic fraction was always the major site of radioactivity deposition (60%), and the time-activity curve of the cytosolic fraction paralleled that of the whole heart throughout the 120-min study period. In the cytosolic fraction, most of the radioactivity was incorporated into the triglyceride class, and the rest was present in the free fatty acid, phospholipid (phosphatidylcholine) and diglyceride classes. In the mitochondrial fraction, the radioactivity was mostly incorporated into the phospholipid class (phosphatidylethanolamine), followed by free fatty acids. The final metabolite of 123I-BMIPP, 123I-p-iodophenylacetic acid (123I-PIPA), initially appeared in the mitochondrial fraction as early as 1 min, and subsequently in the cytosolic fraction at 5 min. Another intermediary metabolite, 123I-p-iodophenyldodecanoic acid (123I-PIPC12), was found only in the mitochondrial fraction after 5 min. In conclusion, the slow washout kinetics of 123I-BMIPP from the myocardium mainly reflects the turnover rate of the triglyceride pool in the cytosol. The BMIPP metabolism, i.e. initial alpha-oxidation followed by subsequent cycles of beta-oxidation, was confirmed in vivo. The participation of the mitochondria in the metabolism was also proven.

Animals↗

PubMed1996

Differential kinetics of [123I]beta-CIT binding to dopamine and serotonin transporters.

Iodine-123-labelled 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid ([123I]beta-CIT) labels both the dopamine transporter (DAT) and the serotonin transporter (5-HTT) and this ligand is able to clarify pathological changes in both dopaminergic and serotonergic systems. However, the differential kinetics of beta-CIT binding to DAT and 5-HTT has not been clarified fully. In this study we examined time-activity curves of [123I]beta-CIT in individual regions in the rat brain. Using cerebellum as the reference region, k3 and k4 values were estimated by a two-compartment kinetic analysis. In the striatum, the kinetics was slowest among all brain areas. In this area specific binding reached its peak 4 h after the injection. In the hypothalamus, specific binding reached its peak 1 h after the injection and its amount did not change until 4 h after the injection. In the occipital cortex, the binding and washout of the ligand were fastest among all brain regions. Estimated k3 values were 0.040+/-0.003 in the striatum, 0.019+/-0.002 in the hypothalamus and 0.082+/-0.011 in the occipital cortex (min-1, mean +/-SD). Estimated k4 values were 0.0034+/-0.0005 in the striatum, 0.0071+/-0.0009 in the hypothalamus and 0.083+/-0.013 in the occipital cortex (min-1, mean +/-SD). Therefore binding kinetics of [123i]beta-cit in the region rich in dat is apparently different from that in the region rich in 5-HTT. These results will provide fundamental data to image both DAT and 5-HTT in one series of examinations with [123I]beta-CIT.

Animals↗

PubMed1996

Prognosis of hypertrophic cardiomyopathy: assessment by 123I-BMIPP (beta-methyl-p-(123I)iodophenyl pentadecanoic acid) myocardial single photon emission computed tomography.

123I-BMIPP (beta-methyl-iodophenyl pentadecanoic acid) has shown unique properties for potential use in assessing myocardial metabolism. Previous basic and clinical studies demonstrated that the disturbances of myocardial metabolism precede the occurrence of myocardial perfusion abnormalities by using 201Tl in hypertrophic myocardium. The present study was therefore undertaken to determine whether or not 123I-BMIPP myocardial SPECT is useful in predicting the prognosis of hypertrophic cardiomyopathy (HCM) in 65 patients in 6 facilities. There were 33 patients with non-obstructive HCM, 12 with obstructive HCM, 12 with apical HCM and 8 with dilated-phase HCM. Fasted patients at rest received an intravenous injection of 111 MBq of 123I-BMIPP. Twenty to thirty minutes later, myocardial SPECT was carried out. The BMIPP severity score (BMIPP SS) was evaluated semiquantitatively by using representative short axial SPECT images. We followed up the incidence of cardiac events for a mean period of 3.0 +/- 0.6 years. Cardiac events occurred in 13 patients. Of these, 11 developed heart failure and 6 died (4 from heart failure and 2 from sudden death). The BMIPP SS in the dilated-phase HCM was significantly lower than that for the nonsurvivors. The BMIPP SS was particularly high in patients with fatal heart failure. Furthermore, there was a close negative correlation between the BMIPP SS and percent fractional shortening measured by echocardiography (r = -0.49). Finally, the mortality over the three years increased according to the extent of the BMIPP SS. In conclusion, these results indicate that BMIPP SS is useful in evaluating the severity of HCM. We conclude that 123I-BMIPP is a valuable metabolic tracer in predicting the outcome of HCM.

Adult↗

PubMed1996

Paradoxical uptake of F-18 fluorodeoxyglucose by successfully reperfused myocardium during the sub-acute phase in patients with acute myocardial infarction.

The myocardial uptake of F-18 fluorodeoxyglucose (FDG) has been shown to indicate ischemia. To elucidate whether this is applicable to reperfused myocardium in patients with acute myocardial infarction (AMI), Tl-201 SPECT and F-18 FDG PET were performed in 10 patients with successfully recanalized AMI (male myocardial perfusion on the infarct-related area was classified, on the basis of Tl-201 images, into 2 groups (normal and defect) during the sub-acute phase, and into 3 grades (normal, redistribution (RD), and persistent defect) during the chronic phase (1 and 3 months after onset). Regional FDG uptake was calculated as FDG uptake in the region of interest normalized relative to that in a normal area. During the chronic phase, FDG accumulated only in the region of RD, indicating ischemia, but during the sub-acute phase, FDG accumulated mainly in the peri-infarct area. To elucidate whether the reperfused myocardium itself shows signs of accelerated glucose uptake, an experimental study was performed in rats. Glucose uptake in the isolated heart was measured by deoxyglucose and 31P-NMR spectroscopy, and was significantly increased after reperfusion compared with the pre-ischemic level. In conclusion, the enhancement of FDG uptake during the sub-acute phase was observed in successfully reperfused myocardium of patients with acute myocardial infarction. Such augmentation disappeared during the chronic phase. An experimental study in rats indicated that ischemia and reperfusion themselves augment glucose uptake. This mechanism may be responsible for the increase in FDG uptake of reperfused myocardium observed clinically.

Aged↗

PubMed1996

Application of interleukin 12 to antitumor cytokine and gene therapy.

In vivo administration of interleukin 12 (IL-12) at 2000 U/mouse induced IL-12-activated killer (IL-12AK) cells in parallel with an elevation in serum interferon-gamma (IFN-gamma) activity. Although NK1.1+CD3- natural killer cells are the major precursor of IL-12AK cells, asialoGM1+CD8+ T-cells were also demonstrated to be novel precursors. Such anomalous killer cells may play an important role in the early stages of the host defense mechanisms against tumors. It was also shown that IL-12 is effective in inducing tumor-specific cytotoxic T-lymphocytes. Consistent with these data, IL-12 had marked activity against various kinds of established tumors when given systemically. Mice cured of tumors by IL-12 treatment acquired tumor-specific T-cell immunity. Moreover, we initially demonstrated that IL-12 was effective in preventing and inhibiting the growth of primary tumors induced by the chemical carcinogen methylnitrosourea using c-Ha-ras transgeneic mice. Finally, we investigated the application of IL-12 to antitumor gene therapy. Transfer of the IL-12 gene into A20 B-lymphoma cells resulted in the continuous production of IL-12 and caused abrogation of in vivo tumorigenicity. Tumor cells transfected with the IL-12 gene are potentially a good tool as a tumor vaccine, as they effectively induced IL-12AK cells, IFN-gamma production, and tumor-specific protective immunity. Although B16-BL-6 melanoma cells, which are a highly metastatic subclone of B16 melanoma cells, showed resistance to IL-12 gene therapy, combination therapy with the B7-1 gene and systemic IL-12 administration almost completely inhibited tumor metastasis. Similar results were obtained using B16-BL-6 melanoma cells transfected with both B7-1 and IL-12 genes. These results suggest that IL-12 is a promising cytokine for antitumor cytokine and gene therapy.

Animals↗

PubMed1996

Cation binding at the node of Ranvier in biopsied peripheral nerves of patients with Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies.

The node of Ranvier in myelinated fibers is known to have an affinity to bind cations. Demyelination and remyelination due to abnormal expression of a myelin protein may affect cation binding or vice versa under pathological conditions. To study the cation binding at the node of Ranvier in inherited demyelinating neuropathies associated with over- and under-expression of the peripheral myelin protein 22 (PMP-22), the reaction with ferric ion and ferrocyanide was used to visualize the cation binding sites in biopsied nerves of four patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and two patients with hereditary neuropathy with liability to pressure palsies (HNPP), and the results were compared with those of four patients having acquired neuropathies with normal PMP-22 expression. In CMT1A, nodal widening or paranodal demyelination was associated with dense precipitates focally on both sides of the widened node. Although fainter precipitates were present at the node between remyelinated internodes, the percentage of nodes exhibiting the reaction product between normal and remyelinated internodes was not statistically different from that between normal internodes in CMT1A. In acquired neuropathies, on the other hand, the difference was significant between the two (P < 0.05), with reduction between normal and remyelinated internodes. At the nodes neighboring demylinated internodes, the percentage of nodes exhibiting the reaction product was reduced significantly in both CMT1A and acquired neuropathies, but to a lesser degree in CMT1A. Precipitates were clearly seen at the nodes neighboring a tomaculum in HNPP. The results suggest that preserved cation binding at the node may allow nerves to keep the electrical excitability in CMT1A and HNPP where myelin remodeling takes place at high frequency.

Adolescent↗

PubMed1996

Alzheimer-type pathology in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).

A 53-year-old Japanese woman with a point mutation in mitochondrial DNA (tRNALeu(UUR), nt3243) consistent with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and Alzheimer-type brain pathology is reported. This woman had suffered myopathy and psychosis without any clinical evidence of, stroke-like episodes during the last 10 years of her life, and had died after an accident. At autopsy 30 h post mortem, a part of the brain was snap frozen for biochemical and histochemical studies, and the remaining part was processed for a routine examination and electron microscopy. In the brain there were no ischemic lesions. Instead, primitive/diffuse senile plaques were found throughout the brain, predominantly in the frontal and temporal lobes, while Alzheimer neurofibrillary tangles were found only in the parahippocampal gyrus. These plaques were positive for beta-protein and mostly negative for tau protein, ubiquitin, neurofilaments, alpha-choline acetyltransferase, and acetylcholinesterase. Mutations in codon 331 of the ND2 gene as well as codons 693, 713 and 717 of the beta-amyloid precursor protein gene, known to be responsible for some cases of familial Alzheimer disease, were not found. Furthermore, coincidental Down syndrome was ruled out by chromosome analysis. The results suggest a possible correlation between this mitochondrial DNA abnormality and Alzheimer-type pathology.

Alzheimer Disease↗

PubMed1996

Accumulation of peripheral myelin protein 22 in onion bulbs and Schwann cells of biopsied nerves from patients with Charcot-Marie-Tooth disease type 1A.

Peripheral myelin protein 22 (PMP-22) is a glycoprotein expressed in the myelin sheath of myelinated Schwann cells. Duplication of the PMP-22 gene and its gene dosage effect have been postulated to be involved in the pathogenesis in the majority of individuals with Charcot-Marie-Tooth disease type 1A (CMT1A). Northern blot analysis has demonstrated that the mean relative ratio of PMP-22 mRNA/beta-actin mRNA in biopsied nerves of patients with CMT1A is significantly higher than that in disease controls. To investigate whether the elevated expression of PMP-22 mRNA is reflected in the amount and the localization of PMP-22, we analyzed PMP-22, myelin basic protein (MBP), protein zero (P0), and S-100 immunoreactivities in biopsied nerves from six patients with CMT1A, five patients with other types of CMT, five patients with acquired demyelinating neuropathies, and two normal subjects. In all patients with CMT other than CMT1A and acquired demyelinating neuropathy, as well as in normal subjects, the myelin sheath was immunoreactive for PMP-22, MBP, and P0, while the Schwann cell cytoplasm was immunoreactive only for S-100. In five out of six patients with CMT1A, however, the PMP-22 immunoreactivity was present not only on the myelin sheath but also in the Schwann cell cytoplasm and onion bulbs (OBs). Although OBs are nonspecific and also seen in other inherited or acquired demyelinating neuropathies, the PMP-22-positive OBs were seen exclusively in CMT1A. The finding suggested that the expression of PMP-22 was abnormal for its localization and probably for the amount in patients with CMT1A carrying duplication of the PMP-22 gene.

Adolescent↗

PubMed1996

Age-related ubiquitin-positive granular structures in non-demented subjects and neurodegenerative disorders.

The distribution and nature of age-related ubiquitin-positive granular structures (UPG) were examined in non-demented brains. In addition, their appearance pattern in some neurodegenerative disorders was investigated. In the transentorhinal cortex, they were distributed among cell islands of layer pre-alpha and in layers II and IIIab. In the amygdala, they were preferentially located in the accessory basal and basal nuclei. UPG were first observed in the transentorhinal cortex of non-demented middle-aged brains and increased in frequency and extended to other regions with increasing age. In Alzheimer-type dementia (ATD), they decreased with advance of the clinical stage. In diffuse Lewy body disease (DLBD), they decreased, accompanying linear neuritic structures. With the double-immuno-staining, UPG were frequently overlapped with neurofilament-positive granules. The multipolar cells of layer pre-alpha and pyramidal cells of layers IIIc and V were also immunostained with anti-neurofilament antibody, and the obliquely ascending fibers of these cells were found frequently to continue to these neurofilament-positive granules. Using ubiquitin immunoelectron microscopy, UPG appeared to derive from degenerating terminal axons. These findings suggest that UPG originate mainly from the recurrent collateral ascending axons in layers II-IIIab and from projecting axons in the amygdala. The occurrence of UPG in the limbic system is an important morphological hallmark of aging. In addition, further studies on the appearance pattern of UPG in ATD and DLBD may clarify whether a difference in the degenerative process of both disorders exists.

Adolescent↗

PubMed1996

Interaction of 2,4,4'-trichloro-2'-hydroxydiphenyl ether with microsomal cytochrome P450-dependent monooxygenases in rat liver.

We studied the effects of 2,4,4'-trichloro-2'-hydroxydiphenyl ether (Irgasan DP300) on the kinetics of the cytochrome P450 (P450)-dependent monooxygenases in rat liver microsomes. The activities of 7-ethoxyresorufin O-deethylase (EROD) and 7-pentoxyresorufin O-depentylase (PROD) in rat liver microsomes exposed to 3-methylcholanthrene (MC) and phenobarbital (PB) respectively, were substantially inhibited by Irgasan DP300. The inhibition profile of EROD was competitive, whereas that of PROD was noncompetitive; the Ki values from Hanes plots were 0.24 and 1.48 microM for EROD and PROD, respectively. Phenacetin O-deethylase (PCOD) and 4-nitrophenol hydroxylase (4NPH) activities in rats exposed to PB were also inhibited by Irgasan DP300, at Ki values lower than those for other microsomes. Irgasan DP300 slightly inhibited testosterone 6 beta-hydroxylase (TS6BH) activities in some microsomes. No effect of Irgasan DP300 on lauric acid omega-hydroxylase (LAOH) activity was evident in any microsomal preparations. These results indicated that Irgasan DP300 inhibits MC- and PB-inducible P450-dependent monoxygenase in vitro competitively or noncompetitively, and that the P450 enzymes of the CYP1A or CYP2B subfamily may contribute to Irgasan DP300 toxicity.

Animals↗

PubMed1996

Antithrombotic effect of topically applied 3-oxa-methano-prostaglandin I1 in the microcirculation and antiplatelet functions of its active form.

The antithrombotic effect of topical application of the 3-oxa-methano-prostaglandin (PG) I1 analog, SM-10902 in the microcirculation and in vitro antiplatelet functions of its active form SM-10906 were estimated in comparison with PGI2 and PGE1. In rat platelets, SM-10906 evoked accumulation of intracellular cyclic adenosine 3',5'-monophosphate, and exhibited antiaggregatory and disaggregatory activities, which were all enhanced by the phosphodiesterase inhibitor theophylline. Additionally, SM-10906 was shown to inhibit platelet adhesion to collagen in human platelet-rich plasma. PGI2 and PGE1 also showed in vitro antiplatelet effects in the order of PGI2 > SM-10906 > or = PGE1. SM-10902 exhibited a dose-dependent anti-thrombotic effect in the guinea pig mesenteric arteriole by a topical application, and this activity might be exerted by the antiplatelet functions of SM-10906. Although SM-10906, PGI2 and PGE1 also showed the antithrombotic effects, SM-10902 was the most potent. In conclusion, the present studies indicate that an external topical preparation of SM-10902 may be useful for the therapy of peripheral circulatory insufficiency.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1996

Expression of dopamine transporter mRNA and its binding site in fetal nigral cells transplanted into the striatum of 6-OHDA lesioned rat.

Neurological disorders in rat model of hemi-Parkinson's disease can be compensated by the transplantation of fetal nigral cells. However, the role of the dopamine transporter (DAT) in this recovery has not been clarified. To clarify this mechanism, we examined the expression of DAT in the caudate putamen (CPu) by in situ hybridization histochemistry (mRNA) and autoradiography (using the ligand [125I] beta-CIT, which labels DAT) and compared them with the recovery of motor disturbance revealed with methamphetamine-induced rotation. Models were made with the stereotaxic injection of 6-hydroxydopamine into the left side of the substantia nigra pars compacta. Cell suspensions from rat fetus (embryonic day 14-15) were transplanted into the lesioned side of CPu. Methamphetamine-induced rotation, expression of DAT mRNA, and [125I] beta-CIT binding were evaluated 2, 4 and 12 weeks after the transplantation. Methamphetamine-induced rotation recovered partly in the 2nd week and significantly in the 4th week. [125I] beta-CIT binding increased with time and the dense binding was detected 4 and 12 weeks after the transplantation. In all transplanted rats, cells expressing DAT mRNA were found in CPu. These results indicated that transplanted fetal dopaminergic cells maturated in CPu of host animals and extended nerve terminals where high density of DAT binding sites were found.

Animals↗

PubMed1996

Structural changes in the intramuscular connective tissue during development of bovine semitendinosus muscle.

Structural changes in the intramuscular connective tissue during development of bovine semitendinosus muscle were investigated using the cell-maceration method for scanning electron microscopy, by which cellular elements were eliminated and collagen fibrils and fibres were exposed. The endomysium was discontinuous and showed various shapes and sizes in the muscle of 7-month fetuses. The perimysium consisted of collagen fibres in loose contact with each other. In the muscle of neonatal calves, the endomysium consisted of cylindrical sheaths and displayed a honeycomb structure, and the perimysium was composed of several layers of collagen fibres. Collagen fibrils in the endomysium bound ever more closely with each other, and collagen fibres in the perimysium increased in thickness, and the wavy pattern of collagen fibres became more regular with growth of cattle. We have examined the mechanical strength of the intramuscular connective tissue by our new method, 'intramuscular connective tissue (IMCT) model'. The IMCT model is composed of collagen fibrils and fibres which maintains the organization in the endomysium and perimysium in situ. The shear-force value of the model increased rapidly from the 7th fetal month to the neonatal stage, and increased linearly with postnatal ageing thereafter. Changes in the arrangement of collagen fibrils and fibres seem to closely related to an increase in the mechanical strength of the intramuscular connective tissue during development of bovine skeletal muscle.

Animals↗

PubMed1996

The effects of proteins on [Ca2+] measurement: different effects on fluorescent and NMR methods.

Previous reports showed that the presence of proteins shifts the apparent dissociation constant (Kd) of a fluorescent dye indicator to Ca2+. To elucidate the sensitivity of Kd of an NMR-sensitive Ca2+ indicator, 5-fluoro-1,2-bis(2-amino-phenoxy)ethane N,N,N'N'-tetraacetic acid (5F-BAPTA) to proteins, and compare with that of a dye indicator, Fura-2, we measured Kd of Fura-2 or 5F-BAPTA using Ca-EGTA buffer with or without proteins. Aldolase (ALD) or bovine cardiac protein (BCP) extracted from bovine hearts was used at concentrations of 10, 25, or 50 mg/ml. ALD significantly increased the apparent Kd of Fura-2 to Ca2+ from 164.1 +/- 5.6 nM (mean +/- SE, N = 8) to 757.2 +/- 2.1 nM (n = 4, P < 0.05) at the concentration of 50 mg/ml. In contrast, Kd of 5F-BAPTA was not markedly changed by ALD (298.4 +/- 3. nM without ALD (n = 8), 385.1 +/- 2.7 nM (n = 4) with 50 mg/ml ALD). BCP (50 mg/ml) also significantly increased Kd of Fura-2 (928.5 +/- 3.3 nM, n = 4, P < 0.05), but did not change Kd of 5F-BAPTA (316.0 +/- 2.9 nM, n = 4). These results indicate that Kd of 5F-BAPTA is much less sensitive to the presence of proteins than Fura-2, and that 19F-NMR coupled with 5F-BAPTA is a more robust method to measure intracellular Ca2+ concentration than a fluorescent method with Fura-2.

Animals↗

PubMed1996

A chronic organized masseter abscess causing trismus resolved by hemi-masseter myotomy.

We present a 62-year-old patient with a chronic organized abscess of the right masseter muscle that developed following parotidectomy. This patient's chronic abscess originated from an infection in the masticator space from the second molar. Cases of repeated parotitis should lead one to suspect a masticator space infection. In this case, the cicatricical masseter muscle produced severe trismus. Total eradication of the abscess and myotomy of the masseter resolved the problem completely. We should pay attention to the dental condition in case of masticator space infection, especially in case of masseter muscle infection mimicking parotitis.

Abscess↗

PubMed1996

Transcription and demethylation of TCR beta gene initiate prior to the gene rearrangement in c-kit+ thymocytes with CD3 expression: evidence of T cell commitment in the thymus.

In order to determine whether the cells immigrating into the thymus have been committed to the T cell lineage, we examined the gene expression of the TCR complex in fetal thymus (FT) and fetal liver (FL) precursors. We previously showed that c-kit bright-positive, Pgp-1 bright-positive and lineage markers negative fetal thymocytes (c-kit+ FT cells) are the most immature cells which do not undergo gene rearrangement of the TCR beta chain. In this study, we demonstrated that the gene rearrangement of TCR gamma as well as beta chains does not occur in c-kit+ FT cells, but that the germline transcript of their TCR beta was found in J-C regions. The TCR beta gene was demethylated in c-kit+ FT cells. CD3 gamma, delta and epsilon subunit genes were also expressed at the mRNA levels in c-kit+ FT cells, but cytoplasmic protein staining divided them into two populations: cytoplasmic CD3 epsilon positive and negative cells. These features were not observed in c-kit+ FL cells. Moreover, Ly-1 expression was found on c-kit+ FT cells but not on c-kit+ FL cells. These results indicate that DNA alteration on the TCR beta gene initiates with other phenotype expression determining the T cell lineage in the thymus prior to TCR gene rearrangement.

Animals↗