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Biomedical subjects

M Tanabe

Publications and source records attributed to M Tanabe.

At least 37 records · Page 2Linked to original sources
PubMed1999

Differentiation of small solitary pulmonary nodules using Tc-99m MIBI and Tl-201 SPECT

The authors evaluated the ability of dual SPECT with Tc-99m MIBI and Tl-201 chloride to differentiate malignant and benign solitary pulmonary nodules smaller than 3 cm in diameter. Forty-three patients had solitary pulmonary nodules smaller than 3 cm in diameter based on the findings of chest CT. All patients underwent dual-isotope SPECT with Tc-99m MIBI and Tl-201 chloride. Regions of interest were placed over the tumors (T) and contralateral normal lung tissue (N) on one coronal SPECT view, and T:N ratios and retention indices were calculated. The sensitivities of early and delayed Tc-99m MIBI SPECT and early and delayed Tl-201 chloride SPECT for differentiating malignant and benign lesions were 44%, 48%, 56%, and 52%, respectively. The corresponding specificity rates were 44%, 56%, 25%, and 31%, respectively, and corresponding accuracy rates were 44%, 51%, 44%, and 44%, respectively. There were no statistically significant differences between malignant and benign lesions in the early and delayed T:N ratios for Tc-99m MIBI and Tl-201 chloride and the retention index for Tc-99m MIBI. However, the retention index using Tl-201 chloride in malignant lesions was significantly higher (P < 0.01) than that in benign lesions. Analysis of semiquantitative parameters of the T:N ratio and retention index from Tc-99m MIBI SPECT appears to have little or no value for differentiating malignant from benign solitary pulmonary nodules smaller than 3 cm in diameter. However, the retention index using Tl-201 chloride seems to be a better parameter for differentiating between these malignant and benign lesions.

Journal Article↗
PubMed1999

Core temperature and sweating onset in humans acclimated to heat given at a fixed daily time.

The thermoregulatory functions of rats acclimated to heat given daily at a fixed time are altered, especially during the period in which they were previously exposed to heat. In this study, we investigated the existence of similar phenomena in humans. Volunteers were exposed to an ambient temperature (Ta) of 46 degrees C and a relative humidity of 20% for 4 h (1400-1800) for 9-10 consecutive days. In the first experiment, the rectal temperatures (Tre) of six subjects were measured over 24 h at a Ta of 27 degrees C with and without heat acclimation. Heat acclimation significantly lowered Tre only between 1400 and 1800. In the second experiment, six subjects rested in a chair at a Ta of 28 degrees C and a relative humidity of 40% with both legs immersed in warm water (42 degrees C) for 30 min. The Tre and sweating rates at the forearm and chest were measured. Measurements were made in the morning (0900-1100) and afternoon (1500-1700) on the same day before and after heat acclimation. Heat acclimation shortened the sweating latency and decreased the threshold Tre for sweating. However, these changes were significant only in the afternoon. The results suggest that repeated heat exposure in humans, limited to a fixed time daily, alters the core temperature level and thermoregulatory function, especially during the period in which the subjects had previously been exposed to heat.

Acclimatization↗
PubMed1999

Apamin-sensitive conductance mediates the K(+) current response during chemical ischemia in CA3 pyramidal cells.

Pyramidal cells typically respond to ischemia with initial transient hyperpolarization, which may represent a neuroprotective response. To identify the conductance underlying this hyperpolarization in CA3 pyramidal neurons of rat hippocampal organotypic slice cultures, recordings were obtained using the single-electrode voltage-clamp technique. Brief chemical ischemia (2 mM 2-deoxyglucose and 3 mM NaN(3), for 4 min) induced a response mediated by an increase in K(+) conductance. This current was blocked by intracellular application of the Ca(2+) chelator, bis-(o-aminophenoxy)-N,N,N', N'-tetraacetic acid (BAPTA), reduced with low external [Ca(2+)], and inhibited by a selective L-type Ca(2+) channel inhibitor, isradipine, consistent with the activation of a Ca(2+)-dependent K(+) conductance. Experiments with charybdotoxin (10 nM) and tetraethylammonium (TEA; 1 mM), or with the protein kinase C activator, phorbol 12,13-diacetate (PDAc; 3 microM), ruled out an involvement of a large conductance-type or an apamin-insensitive small conductance, respectively. In the presence of apamin (1 microM), however, the outward current was significantly reduced. These results demonstrate that in rat hippocampal CA3 pyramidal neurons an apamin-sensitive Ca(2+)-dependent K(+) conductance is activated in response to brief ischemia generating a pronounced outward current.

ATP-Binding Cassette Transporters↗
PubMed1999

Avulsion fracture of the anterior half of the foramen magnum involving the bilateral occipital condyles and the inferior clivus--case report.

A 38-year-old male presented with an avulsion fracture of the anterior half of the foramen magnum due to a traffic accident. He had palsy of the bilateral VI, left IX, and left X cranial nerves, weakness of his left upper extremity, and crossed sensory loss. He was treated conservatively and placed in a halo brace for 16 weeks. After immobilization, swallowing, hoarseness, and left upper extremity weakness improved. Hyperextension with a rotatory component probably resulted in strain in the tectorial membrane and alar ligaments, resulting in avulsion fracture at the sites of attachment, the bilateral occipital condyles and the inferior portion of the clivus. Conservative treatment is probably optimum even for this unusual and severe type of occipital condyle fracture.

Accidents, Traffic↗
PubMed1999

Effects of thromboxane synthetase inhibitor (RS-5186) on experimentally-induced cerebral vasospasm.

RS-5186, which inhibits thromboxane A2 (TXA2) synthetase activity, ameliorated delayed cerebral vasospasm in a canine two-hemorrhage model. Subarachnoid hemorrhage was induced in 15 dogs, which were divided into two groups. In the RS-5186-treated group (9 dogs), 50 mg kg-1 of RS-5186 was administered twice a day for seven days. The remaining six dogs without administration of RS-5186 were used as a control group. In the RS-5186-treated group, the angiographic diameter of the basilar artery on Day 7 after subarachnoid hemorrhage was constricted to 60.9% +/- 11.6% (n = 9, mean +/- SD) of that on Day 0, before subarachnoid hemorrhage. The corresponding value was 42.8% +/- 6.1% (n = 6) in the control group. There was a statistically significant difference between these percentages. In the RS-5186-treated group, plasma thromboxane B2 level on Day 7 was 144.3 +/- 28.1 pg ml-1 (n = 4), which was lower than the 815.5 +/- 162.0 pg ml-1 (n = 4) in the control group (p < 0.0005). The plasma 6-keto-prostaglandin F1 alpha level on Day 7 was 180.5 +/- 66.5 pg ml-1 (n = 4) in the RS-5186-treated group, and higher than 107.3 +/- 12.4 pg ml-1 (n = 4) in the control group (p = 0.0734). Thus, administration of RS-5186 reduced TXA2 plasma level and had a beneficial effect on angiographically-detected delayed vasospasm.

Animals↗
PubMed1999

[Recent clinical trials for sepsis: analysis of the results and future perspectives].

Recent clinical trials with experimental immunotherapeutic agents for sepsis have not proven their overall benefit yet although some studies suggested significant effect of these antisepsis therapies. This review article summarizes the results of these trials, their analysis, lessons learned from past failure, and future perspectives for immunotherapies as anti-sepsis treatments.

Animals↗
PubMed1999

Soft-wall reconstruction of posterior canal wall for surgery of noninflamed ears: a preliminary report.

OBJECTIVE: To test whether the posterior external auditory canal (EAC) wall reconstructed only by soft tissues retracts after surgery in the noninflamed ear. STUDY DESIGN: The condition of the posterior EAC wall was observed for more than 1 year after surgery in 20 noninflamed ears in which only the posterior EAC wall skin was preserved or in which the wall was reconstructed only by soft tissue during surgery. PATIENTS: Eighteen patients (20 ears) underwent ear surgery for conditions other than otitis media, including ossiculoplasty in 12 ears, cochlear implant in 3, resection of congenital cholesteatoma in 4, and resection of glomus tympanicum tumor in 1. RESULTS: Retraction of the soft posterior EAC wall was observed in only 1 of the 20 ears. In this ear, the posterior EAC wall showed only a slight retraction without any serious problems. Computed tomography revealed that mastoid aeration recovered in all 20 ears. CONCLUSIONS: In noninflamed ears, surgeons can remove the bony posterior EAC wall if necessary, and may not need to reinforce or reconstruct the wall with hard tissue. This enables surgeons to spare time and energy and obtain the same advantages as in the intact-canal-wall technique or canal wall reconstruction by a hard material.

Adolescent↗
PubMed1998

Proteasome inhibition leads to the activation of all members of the heat-shock-factor family.

Heat-shock proteins and molecular chaperones are involved in various cellular metabolic processes including protein synthesis and degradation. These expressions are elevated at the level of transcription by the accumulation of abnormal proteins when these metabolic processes are disturbed. Recent works suggest the induction of heat-shock proteins by the inhibiton of proteasome. To elucidate the mechanism of this induction, we examined the activation of heat-shock transcription factors by proteasome inhibitors in avian cells. Activation of the two heat-shock-inducible factors, HSF1 and HSF3, was produced by the treatment of cells with proteasome inhibitors. This activation was not produced by treatment with various other protease inhibitors. The HSF activation by proteasome inhibitors was completely blocked in the presence of the protein synthesis inhibitor cycloheximide. Unexpectedly, the development-related factor HSF2 was also activated by proteasome inhibitors, with an increase in its protein level. These results suggest that the ubiqutin-proteasome pathway may regulate all of the three HSFs by controlling the level of some regulatory factor for HSF or HSF itself, as well as controlling abnormal proteins.

Animals↗
PubMed1998

Neuronal src and trk a protooncogene expression in neuroblastomas and patient prognosis.

Neuroblastomas present a wide variety of clinical and biological behaviors, which are reflected by the heterogeneous expressions of protooncogenes related to the neuronal differentiation and amplification of the N-myc gene. High expression of trk A and Ha-ras in neuroblastomas has been shown to be associated with an excellent patient outcome. We have previously reported that neuron-specific src mRNA was increased in chemically differentiated neuroblastoma cell lines and in clinically observed neuroblastomas without N-myc amplification. In the present study, to clarify both the value of neuronal c-srcN2 expression as a prognostic indicator and the significance of the coexpression of these protooncogenes, we examined the expression of 3 alternatively spliced src, trk A and Ha-ras in neuroblastoma tissues from 60 patients by competitive RNA-polymerase chain reaction (PCR). The results indicate that protooncogene expression in neuroblastomas correlated with a favorable outcome for c-srcN2 and trk A. N-myc gene was amplified exclusively in tumors with low levels of trk A. Low expression of c-srcN2 and trk A might thus characterize different aggressive phenotypes due to different signal transduction pathways of neural differentiation in neuroblastoma. The combined analyses for c-srcN2 and trk A expression by RNA-PCR should provide information about the biological phenotype of a neuroblastoma within a short period of time after obtaining tumor material.

Genes, myc↗
PubMed1998

Glial cell line-derived neurotrophic factor/neurturin-induced differentiation and its enhancement by retinoic acid in primary human neuroblastomas expressing c-Ret, GFR alpha-1, and GFR alpha-2.

Neuroblastomas often undergo spontaneous differentiation and/or regression in vivo, which is at least partly regulated by the signals through neurotrophins and their receptors. Recently, glial cell line-derived neurotrophic factor (GDNF) and a second family member, neurturin (NTN), have been found to mediate their signals by binding to a heterotetrameric complex of c-Ret tyrosine kinase receptors and glycosylphosphatidylinositol-linked proteins, GFR alpha-1 (GDNFR-alpha) or GFR alpha-2 (TrnR2/GDNFR-beta/NTNR-alpha/RETL2). Here, we studied the effect of GDNF and NTN on human neuroblastomas in the short-term primary culture system, as well as the expression of c-Ret, GFR alpha-1, GFR alpha-2, GDNF, and NTN. GDNF (1-100 ng/ml) induced morphological differentiation in 34 of 38 primary neuroblastomas and an accompanying increase in c-Fos induction. These effects were markedly enhanced by treatment with 5 microM all-trans-retinoic acid. Although GDNF alone induced a rather weak differentiation independent of the disease stages, the enhancement of neurite outgrowth induced by treatment with both GDNF and all-trans-retinoic acid was significantly correlated with younger age (less than 1 year; P = 0.0039), non-stage 4 diseases (P = 0.0023), a single copy of N-myc (P = 0.027), and high levels of TRK-A expression (P = 0.0062). To examine the expression levels of GFR alpha-1, we cloned a short form of the human GFR alpha-1 gene with a 15-bp deletion by screening a human adult substantia nigra cDNA library. Many primary neuroblastomas expressed c-Ret, GFR alpha-1, and GFR alpha-2 as well as their ligands, GDNF and NTN, suggesting the presence of a paracrine or autocrine signaling system within the tumor tissue. The effect of NTN on primary culture cells of neuroblastoma was similar to that of GDNF. These imply that the GDNF(NTN)/c-Ret/GFR alpha-1(GFR alpha-2) signaling may have an important role in regulating the growth, differentiation, and cell death of neuroblastomas.

Antineoplastic Agents↗
PubMed1998

Disruption of the HSF3 gene results in the severe reduction of heat shock gene expression and loss of thermotolerance.

The vertebrate genome encodes a family of heat shock factors (HSFs 1-4) of which the DNA-binding and transcriptional activities of HSF1 and HSF3 are activated upon heat shock. HSF1 has the properties of a classical HSF and exhibits rapid activation of DNA-binding and transcriptional activity upon exposure to conditions of heat shock and other stresses, whereas HSF3 typically is activated at higher temperatures and with distinct delayed kinetics. To address the role of HSF3 in the heat shock response, null cells lacking the HSF3 gene were constructed by disruption of the resident gene by somatic recombination in an avian lymphoid cell line. Null cells lacking HSF3, yet expressing normal levels of HSF1, exhibited a severe reduction in the heat shock response, as measured by inducible expression of heat shock genes, and did not exhibit thermotolerance. At intermediate heat shock temperatures, where HSF1 oligomerizes to an active trimer in wild-type cells, HSF1 remained as an inert monomer in the HSF3 null cell line. HSF3 null cells were restored to a nearly normal heat shock-responsive state by reintroduction of an exogenous HSF3 gene. These results reveal that HSF3 has a dominant role in the regulation of the heat shock response and directly influences HSF1 activity.

Animals↗