Adnexal polyp of neonatal skin observed beyond the neonatal period.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Koizumi.
Explore the source record for details and available documents.
A method is proposed for extracting target dipolesource activities from two sets of evoked magnetoencephalographic (MEG) data, one measured using task stimuli and the other using control stimuli. The difference matrix between the two covariance matrices obtained from these two measurements is calculated, and a procedure similar to the MEG-multiple signal classification (MUSIC) algorithm is applied to this difference matrix to extract the target dipole-source configuration. This configuration corresponds to the source-configuration difference between the two measurements. Computer simulation verified the validity of the proposed method. The method was applied to actual evoked-field data obtained from simulated task-and-control experiments. In these measurements, a combination of auditory and somatosensory stimuli was used as the task stimulus and the somatosensory stimulus alone was used as the control stimulus. The proposed covariance difference analysis successfully extracted the target auditory source and eliminated the disturbance from the somatosensory sources.
We investigated the relationship between hemodynamic changes in the cortex measured by near-infrared spectroscopy (NIRS) and the polysomnographic changes during sleep. Four healthy male volunteers participated in the study. Near-infrared spectroscopy measuring and polysomnographic recordings were done simultaneously during sleep. In many case, oxy-hemoglobin (oxy-Hb) decreased and deoxy-hemoglobin (deoxy-Hb) increased during the transition from wakefulness to sleep, and oxy-Hb increased toward deep sleep. Oxy-Hb and deoxy-Hb had larger fluctuations during REM sleep than those during non-REM sleep. During REM sleep, oxy-Hb often showed a lower level and deoxy-Hb showed a higher level than those during the preceding and following non-REM sleep.
The Trk family of tyrosine protein kinase receptors plays a significant role in the development and maintenance of neural tissues. It has been recently shown that Trk receptors are also expressed by a wide range of normal non-neuronal tissues in humans in a cell type-specific manner. In the present study, the expression patterns of TrkA in 337 non-neuronal invasive carcinomas of 15 different human tissues were investigated immunohistochemically. Overall, 133 (39%), 101 (30%) and 103 (31%) tumors exhibited strong, moderate and no TrkA immunoreactivity, respectively. Esophageal and thyroid carcinomas expressed high levels of TrkA, whereas the levels in gastric and colon cancers were low. TrkA expression was detected not only in carcinomas originating from TrkA-positive normal counterpart tissues, including the esophagus, breast, lung and uterus, but also in those from TrkA-negative tissues/cells of the thyroid, liver and ovary. Immunostaining for nerve growth factor-beta, the specific ligand for TrkA, in esophageal and breast carcinomas demonstrated its immunoreactivity in stromal fibroblasts and some TrkA-expressing tumor cells. These results suggest that paracrine/autocrine regulation via stromal/tumoral NGF-tumoral TrkA interaction may be involved in the growth of certain non-neuronal carcinomas.
Carcinogenicity testing is indispensable for identifying environmental carcinogens and for evaluating the safety of drugs in the process of development. Conventional 2-year rodent bioassays are one of the most resource-consuming tests in terms of animals, time, and costs. Development of rapid carcinogenicity testing systems that can assess carcinogenicity within a short period has become a social demand and is essential to improve efficacy in the identification of environmental carcinogens as well as in the development of new drugs. In this review we introduce the rapid carcinogenicity testing system using transgenic (Tg) mice carrying the human prototype c-Ha-ras gene, namely rasH2 mouse (CB6F1-TgHras2 mouse is the same mouse). The studies have been conducted to validate the rasH2 mouse as a model for the rapid carcinogenicity testing system. Our current validation studies revealed that rasH2 mice are able to detect various types of mutagenic carcinogens within 6 months. The rasH2 mice may also be able to detect various nonmutagenic carcinogens. The validation studies also revealed that rasH2 mice are generally much more susceptible to both mutagenic and nonmutagenic carcinogens than control non-Tg mice. No significant tumor induction has been observed in rasH2 mice with either mutagenic or nonmutagenic noncarcinogens. More rapid onset and higher incidence of more malignant tumors can be expected with a high probability after treatment with various carcinogens in the rasH2 mice than in control non-Tg mice. The rasH2 mouse appears to be a promising candidate as an animal model for development of a rapid carcinogenicity testing system.
OBJECT: Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically, this protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBI in rats. METHODS: Male Sprague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the amyloid precursor protein (APP), a marker of axonal injury. The density of APP-marked damaged axons within the corticospinal tract at the pontomedullary junction was calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05). CONCLUSION: The authors infer from these findings that early as well as delayed posttraumatic hypothermia results in substantial protection in TBI, at least in terms of the injured axons.
Recently, spinal cord stimulation (SCS) has been used for the treatment of patients in prolonged coma. However, the results of SCS in unresponsive patients with hypoxic encephalopathy at the chronic stage have not been satisfactory. Considering these circumstances, we began SCS from one month after the onset of hypoxic encephalopathy and evaluated its effect. Twelve patients (5 males and 7 females) with hypoxic encephalopathy, ranging in age from 7 to 72 years, were treated with SCS. The causes of hypoxia were acute cardiac failure in 4, automobile exhaust gas poisoning in 2, and asthma, pneumothorax, anaphylaxis, asphyxia, drowning and hypotension during aortic surgery in one patient each. One month after the onset, an electrode for electrical stimulation was implanted in the epidural space at the C2-C4 level under general anesthesia. The spinal cord was stimulated for 8 hours each day, starting on the day after implantation, and was continued for 3 months. Magnetic resonance imaging (MRI), cerebral blood flow (CBF) measurement using xenon-computed tomography (Xe-CT), and measurement of auditory evoked potential (AEP) and somatosensory evoked potential (SEP) were carried out 3 weeks after the onset for presurgical evaluation. Among the 12 patients, 7 (58%) showed clinical improvement, beginning within two weeks after starting stimulation. They were able to communicate with others and to express their emotion. However, disturbance of writing, picture drawing and calculation were not improved by stimulation. From presurgical evaluation, cases in which SCS therapy was effective had the following features: 1) No hemorrhagic infarction in the basal ganglia was demonstrable by MRI. 2) Mean hemispheric CBF measured by the Xe-CT method exceeded 25 ml/100 g per min. 3) The mean increase in hemispheric CBF 20 min after acetazolamide administration exceeded 5 ml/100 g per min. 4) An N20 peak was evident on the median nerve SEP, SCS appears to be an effective supplementary for unresponsive patients with hypoxic encephalopathy at the subacute stage, in addition to rehabilitation and drug therapy.
Telomerase is a specific enzyme required for the replication of telomeres. Its activity is detected in almost human cancers. We examined in esophageal carcinoma and lesions unstained with Lugol's solution telomerase activity by using telomeric repeat amplification protocol (TRAP) assay. Telomerase activity was detected in all 22 esophageal carcinomas, regardless of histopathological findings. In unstained lesions, telomerase activity was detected in 15 of 22; 10 squamous cell carcinomas, four dysplasia, one regenerative epithelium, no telomerase activity was found in seven; four normal esophageal epithelia, two Barrett's esophagi, one regenerative epithelium. These results suggest that telomerase activity may be a useful molecular marker for the diagnosis of esophageal carcinoma and of the early esophageal carcinoma in area unstained with Lugol's solution.
A case of prostatic rhabdomyosarcoma in an 8-year-old boy is presented. He was referred to Kurobe City Hospital with chief complaints of urinary retention and fever. Radiologic examinations revealed a huge prostatic tumor. Prostatic needle biopsy was performed and the pathological diagnosis was embryonal rhabdomyosarcoma of the prostate. He was referred to our hospital and treated with chemotherapy consisting of cisplatin, vincristine, cyclophosphamide, adriamycin, actinomycin-D and radiotherapy based on the regimen of IRS III. Total prostatectomy was performed 6 months after the start of therapy. Viable tumor cells were found in the prostate and the left obturator lymph nodes. After the operation, we continued chemotherapy. No recurrence was observed 8 months after the operation. However, local recurrence occurred in the pelvis 10 months after the operation and he died 2 months after the recurrence.
The mechanism of hypothermic cerebroprotection after traumatic brain injury (TBI) is unknown. The present study was conducted to investigate the effects of mild hypothermia on the changes in cortical extracellular amino acids and cerebral blood flow (CBF) caused by cerebral contusion created in the rat parietal cortex by a weight-drop method. CBF in both normothermia (37 degrees C) and hypothermia (32 degrees C) groups, which was monitored using the hydrogen clearance technique, decreased significantly after contusion, but never fell below the threshold for ischemia. Cortical levels of glutamate, aspartate, glycine and taurine, which were measured by intracerebral microdialysis, were significantly increased after contusion in each group. However, these increases were greater in the hypothermic than in the normothermic rats. Normal plasma amino acid levels were high, and autoradiography following intravenous injection of 14C-labeled glutamate revealed marked extravasation of [14C]glutamate at the site of cortical impact. These results suggest that the post-traumatic increase in extracellular amino acids occurs independently of CBF reduction, and that extravasation of amino acids from the vascular compartment partly contributes to this increase. Hypothermic cerebroprotection in TBI is thus likely to occur through a mechanism other than reduction in interstitial excitatory amino acids. In TBI, it is postulated that the postsynaptic effects of hypothermia may be more important than the presynaptic effects, when CBF is kept above the ischemic threshold.
Explore the source record for details and available documents.
Vitamin D3 is a new therapeutic agent for psoriasis. Hyperproliferation of epidermis and over-secretion of IL-8 by keratinocytes are the characteristic features of psoriasis. The present study was conducted to determine whether a new vitamin D3 analogue, 22-oxacalcitriol, could be effective in inhibiting the proliferation and IL-8 secretion of normal human epidermal keratinocytes. Cell proliferation was measured colorimetrically by the MTS assay. IL-8 secretion was measured with ELISA. Proliferation of cultured normal human epidermal keratinocytes was inhibited in the presence of 1,25-dihydroxyvitamin D3 at the concentrations of 1 x 10(-8) to 1 x 10(-6) M and 22-oxacalcitriol at concentrations of more than 1 x 10(-9) M at 48 h. IL-8 secretion from normal human epidermal keratinocytes was augmented by TNF-alpha, or synergistically by TNF-alpha and IFN-gamma. 1,25-Dihydroxyvitamin D3 and 22-oxacalcitriol inhibited cytokine-stimulated IL-8 production dose dependently after 24 h incubation without inhibition of cell proliferation. 1,25-Dihydroxyvitamin D3 and 22-oxacalcitriol are considered to inhibit the proliferation of keratinocytes directly and indirectly with inhibition of the secretion of IL-8 from keratinocytes. The inhibition of IL-8 secretion from keratinocytes by vitamin D3 could modulate the behaviour of immunocompetent cells infiltrating in the skin.
The control of cell survival and cell death is of central importance in tissues with high cell turnover such as the lymphoid system. We have examined the effect of cytokines on IL-2 deprivation-induced apoptosis of human antigen-specific T helper clones with different cytokine production profiles. We found that IL-2, interferon-alpha (IFN-alpha), and IFN-beta inhibited IL-2 deprivation apoptosis in Th0, Th1, and Th2 clones. We also found that IL-2 protects T cell clones from IL-2 deprivation apoptosis accompanying active proliferation and enhanced expression of P53, Rb and Bcl-xL proteins. In contrast, IFN-alpha/beta rescued T cell clones from apoptosis without active proliferation, and expression of apoptosis-associated proteins tested so far was unaffected. This may be due to the fact that T cells treated with IL-2 contained those located in S + G2/M phases of the cell cycle, whereas the vast majority of T cells treated with IFN-alpha/beta were located in G0/G1 phase. IFN-alpha/beta specifically induced tyrosine phosphorylation and translocation into nucleus of signal transducers and activators of transcription (STAT) 2 protein in the T cell clones. In addition, over-expression of STAT2 by transfection of the cDNA prevented apoptosis of the T cell clones. Our present study shows that IFN-alpha and -beta mediate anti-apoptotic effect through other pathways than that of IL-2 in growth factor deprivation apoptosis.
The exact mechanism of hypothermic cerebroprotection after traumatic brain injury (TBI) is not fully understood. The present study was conducted to investigate the effects of mild hypothermia on trauma-induced synthesis of nitric oxide (NO), which has been implicated in the pathogenesis of ischemic brain damage associated with glutamate neurotoxicity. Cerebral contusion was created in the rat parietal cortex by a weight-drop method, and extracellular concentrations of the NO end products nitrite and nitrate were measured using in vivo brain microdialysis and capillary electrophoresis under normothermic (37 degrees C) and mild hypothermic (32 degrees C) conditions. In normothermic animals, the level of NO end products increased markedly 10 min after contusion, reaching a maximum level at 20 min. In the hypothermic rats, such increases were absent. Although it is unknown whether endothelial NO synthase, neuronal NO synthase, or both caused the elevation of the NO end products seen in the normothermic animals, the present results indicate that inhibition of NO synthesis may play a part in hypothermic cerebroprotection following TBI.
This paper proposes a method of localizing multiple current dipoles from spatio-temporal biomagnetic data. The method is based on the multiple signal classification (MUSIC) algorithm and is tolerant of the influence of background brain activity. In this method, the noise covariance matrix is estimated using a portion of the data that contains noise, but does not contain any signal information. Then, a modified noise subspace projector is formed using the generalized eigenvectors of the noise and measured-data covariance matrices. The MUSIC localizer is calculated using this noise subspace projector and the noise covariance matrix. The results from a computer simulation have verified the effectiveness of the method. The method was then applied to source estimation for auditory-evoked fields elicited by syllable speech sounds. The results strongly suggest the method's effectiveness in removing the influence of background activity.
Phenotypic and functional properties of gammadelta T cells, which play an important role in mucocutaneous immunity, were examined to elucidate whether immunological abnormality in Behcet's disease may be related to a specific T cell population. We found that CD45RA+ Vgamma9+ Vdelta2+ gammadelta T cells, which constitute a minor population of gammadelta T cells in healthy individuals, were increased in number in Behçet's disease irrespective of disease activity. This CD45RA+ subset of gammadelta T cells in the active, but not inactive, phase of this disease expressed IL-2Rbeta and HLA-DR, suggesting that they are activated in vivo in active Behçet's disease. In addition, the CD45RA+ gammadelta T cells produced extreme amounts of tumour necrosis factor and contained perforin granules. These data indicate that a phenotypically distinct subset of gammadelta T cells, CD45RA+ CD45RO- Vgamma9+ Vdelta2+, may contribute to immunological abnormalities which may lead to complexity of pathophysiology in Behçet's disease.
Epidermal keratinocytes express beta 2-adrenergic receptors on the cell membrane. The binding of the agonists to the beta 2-adrenergic receptors regulates activation of adenylate cyclase. This transmembrane signaling system has been regarded to be one of the important pathways for the functions of keratinocytes. We previously reported that beta-adrenergic stimulation induced a transient increase of intracellular Ca2+ in normal human epidermal keratinocytes. Thus we investigated the effects of epinephrine on another transmembrane signaling system, the phosphatidyl-inositol signal transduction pathway in pig epidermis. Treatment of pig pure epidermis with epinephrine resulted in a transient increase in inositol 1,4,5-trisphosphate with a peak at 30 s. Epinephrine induced translocation of protein kinase C from cytosol to the membrane fraction. The activation of protein kinase C, translocation of protein kinase C from cytosol to the membrane fraction, was confirmed using the beta-adrenergic agonist isoproterenol. Moreover, the effect of epinephrine on the activation of protein kinase C was inhibited by preincubation with propranolol, a beta-adrenergic antagonist. The increase in inositol 1,4,5-trisphosphate and translocation of protein kinase C by epinephrine are consistent with the view that beta-adrenergic stimulation induces turnover of inositol phospholipid in pig epidermis.
We experienced a case of adenocarcinoma occurring in the reconstructed bladder 38 years after ileocystoplasty. The patient was a 48-year-old woman, who had undergone ileocystoplasty and left nephrectomy at the age of 10 for the treatment of tuberculous contracted bladder and left renal tuberculosis. She had often suffered from right pyelonephritis following the operation. She visited our hospital for work-up of a high value of carcinoembryonic antigen (CEA). The findings of cystoscopy, cystogram and urine cytology showed a malignant tumor of the reconstructed bladder. Then, we performed total cystectomy and right ureterostomy. The histopathological examination showed that the tumor was an adenocarcinoma which developed mainly from the ileal segment of the reconstructed bladder.