Biomedical subjects
T Kondoh
Publications and source records attributed to T Kondoh.
MRI and arthroscopic findings in the temporomandibular joint after mandibulectomy including the unilateral condyle. Report of two cases.
In this report, the MRI and arthroscopic findings in the temporomandibular joint (TMJ) of two patients who underwent partial mandibulectomy including the condyle are presented. The disc and superior joint compartment of the affected TMJs were preserved in both patients. MRI of the affected TMJs without condyle demonstrated that the intermediate zone of the discs was located anteriorly to the summit of the articular eminence. Joint effusion was detected in the superior joint compartment of one patient. Fibrous adhesions were observed arthroscopically in the superior joint compartment of both affected TMJs. In contrast, no specific findings were demonstrated in the contralateral TMJs connected with the residual mandibular fragment.
Ischemic "cross" tolerance in hypoxic ischemia of immature rat brain.
The phenomenon of ischemic tolerance has been closely associated with the expression of heat shock proteins but recently, stress tolerance not related to hsp72 has been reported. In the present study, we focused on ischemic tolerance induced by hypoxia and hyperthermia in neonatal rat brain and analyzed the expression of hsp72. In a neonatal rat model of hypoxic ischemia (H-I), preconditioning by whole-body hyperthermia or hypoxia was induced 24 h prior to the ischemia. Brain damage was histologically evaluated and the expressions of hsp72 were analyzed. Hyperthermic preconditioning at 41 degrees C for 15 min, as well as hypoxic preconditioning with 8% hypoxia for 3 h, had almost complete neuroprotective effects. However, we failed to detect the expression of hsp72 in any of preconditioning. Only the H-I insult itself induced hsp72 in the dorsal striatum and slightly in the thalamus and the hippocampus. Hyperthermic preconditioning has neuroprotective effects which are comparable to hypoxic preconditioning in immature brain. The expression of hsp72 is not likely necessary for the ischemic tolerance in immature brain.
Synergistic effect of PTH on the mechanical responses of human alveolar osteocytes.
The aim of this study is to characterize the response of alveolar osteocytes to stretching and parathyroid hormone, (1-34) PTH. Osteocytes from primary human alveolar bone were used in the study. Compared to osteoblasts, osteocytes were observed to express lower levels of alkaline phosphatase mRNA and higher levels of osteocalcin mRNA. We found that the effect of PTH and stretching on osteocalcin expression is synergistic. The upregulated steady-state level of osteocalcin mRNA is further upregulated in the presence of PTH (at 1 h after the initiation of stretching). On the other hand, the downregulated level of the message is further downregulated in the presence of PTH (at 3 h after the 3-h stretching). The synergy can be either way, positive or negative, in the course of the response. From this, we presume that related mechanisms are at work between the PTH signaling pathways and the mechanotransduction pathways activated by stretching.
Store Ca2+ depletion enhances NMDA responses in cultured human astrocytes.
NMDA produced whole-cell membrane currents in cultured human astrocytes. The currents were not inhibited by the selective NMDA receptor antagonist, APV, while they were partially inhibited by the broad G-protein inhibitor, GDPbetaS. NMDA-induced currents were enhanced by either the microsomal Ca2+/ATPase inhibitors, thapsigargin and cyclopiazonic acid, or the ATP-uncoupler, dinitrophenol (DNP). In the Ca2+ assay, NMDA increased intracellular calcium concentration. The increase was inhibited by 26% in Ca2+-free extracellular solution, and it was not inhibited by APV. The results of the present study suggest that NMDA responses in human astrocytes are regulated by store Ca2+ depletion-associated signal.
Intraoperative radiation therapy for metastatic spinal tumors.
STUDY DESIGN: Retrospective examination of 37 patients with metastatic spinal tumors treated with intraoperative radiation therapy. OBJECTIVE: To propose a new technique for local control of metastatic spinal tumors. SUMMARY OF BACKGROUND DATA: No reports of intraoperative radiation therapy for metastatic spinal tumors have been published as of the time of this writing. METHODS: Between December 1992 and April 1996, intraoperative radiation therapy was performed in 37 patients with spinal metastasis. In all but one patient, the spinal cord was protected during intraoperative radiation therapy by a lead shield to prevent radiation myelopathy. In addition to intraoperative radiation therapy, 22 of the 37 patients received external radiation therapy, either before or after their operation. Although the authors had recommended a dose of approximately 30 Gy of external radiation therapy after wound suture removal to patients who did not receive preoperative radiation therapy, the remaining 15 patients did not receive external radiation therapy, either by choice or because they received alternative therapy. Adjuvant chemotherapy for various cancers was administered to 9 of the 37 patients, including 4 of the aforementioned 15. RESULTS: All patients attained clinical improvement in pain, neurologic function status, or both, with no evidence of local recurrence. Radiation myelopathy developed in the one patient whose spinal cord was not protected during intraoperative radiation therapy. Eleven patients experienced metastasis in vertebrae that were not surgically treated. CONCLUSION: Intraoperative radiation therapy appears to achieve good palliation and may be useful for local control of spinal metastases.
Autosomal dominant onychodystrophy and congenital sensorineural deafness.
The disease "deafness and onychodystrophy" (DOD) is characterized by congenital hearing impairment and dystrophic or absent nails and teeth. The autosomal dominant form of the disorder has been previously reported only in one family. We describe here another family in which three members in three generations (a girl, her mother, and her maternal grandfather) were affected with DOD. Our finding is consistent with an autosomal dominant mode of inheritance and confirms autosomal dominant DOD (DDOD, MIM *124480) as a recognizable clinical entity.
Non-traumatic acute paraplegia associated with cervical disc herniation: a case report.
BACKGROUND: Acute paraplegia attributable to disc herniation is known to occur most frequently at the thoracic level. We report a rare case of non-traumatic acute paraplegia caused by disc herniation at the cervical level. Preoperative magnetic resonance imaging (MRI) of the present case demonstrated a spinal cord lesion as a cause of paraplegia. Although this symptom is believed to disappear rapidly after surgical treatment, there have been a few reported cases with poor neurologic recovery and permanent deficits. CASE DESCRIPTION: A 61-year-old female with a history of minor neck pain suffered from non-traumatic acute paraplegia attributable to cervical disc herniation. She underwent emergency surgery consisting of vertebrectomy, removal of herniated discs, and anterior fusion. Postoperative neurologic improvement was slow due to the cervical spinal cord lesion at the central portion of the cord, which was detected by the preoperative and postoperative MRIs. CONCLUSION: We emphasize that the MRI study is crucial for the management of patients with acute neck pain associated with cervical canal stenosis. Surgical treatment should not be delayed to avoid permanent neurologic deficits. Anterior decompression with vertebrectomy is recommended to decompress the injured spinal cord in the narrow cervical spinal canal; however, a cord lesion detected by MRI may indicate an incomplete surgical outcome.
Ubiquitin-like polypeptide inhibits the proliferative response of T cells in vivo.
The monoclonal nonspecific suppressor factor (MNSF), a lymphokine produced by murine T cell hybridoma, possesses pleiotrophic Ag-nonspecific suppressive functions. Recently, we demonstrated that the recombinant form of the ubiquitin-like segment (rUbi-L) of MNSFbeta, a 15.6 kDa-protein consisting of a polypeptide with 36% homology with ubiquitin fused to the ribosomal protein S30, presented an antigen-nonspecific immunoregulatory action in a manner similar to native MNSF. Although this cytokine has been characterized in vitro, little is known about its effects in vivo. Thus, we investigated whether rUbi-L shows a suppressor activity in vivo. The proliferative response of Con A (5 microg/ml)-stimulated splenocytes of mice treated with rUbi-L (500 ng/body) was notably decreased in a dose-dependent manner (max. 57+/-20%). In contrast, administration of high dose ubiquitin (50 microg/body) showed a little, but significant, effect (30+/-7%). Interestingly, concomitant addition of ubiquitin inhibited Ubi-L-induced suppression. Mice injected with rUbi-L without gelatin did not show any suppressive effect. NA4 (1microg/body), a neutralizing monoclonal antibody against rUbi-L, abolished the Ubi-L-mediated suppression. Therefore, ubiquitin-like polypeptide may be implicated in the immune responses in vivo.
Association between arthroscopic diagnosis of temporomandibular joint osteoarthritis and synovial fluid nitric oxide levels.
OBJECTIVE: The purpose of this study was to determine whether there is a relationship between synovial fluid levels of nitric oxide and clinical and arthroscopic findings of synovitis or cartilaginous degeneration. STUDY DESIGN: Arthroscopic surgery was performed on 20 joints in 15 female patients with internal derangement and osteoarthritis of the temporomandibular joint. Synovial fluid aspirates were obtained immediately before arthroscopy. Synovial fluid was also obtained from 14 joints of 11 female asymptomatic volunteers. The concentration of nitrite in the fluid recovered from each temporomandibular joint was measured through use of a highly sensitive and specific chemiluminescence detection method, calibrated per 1 mg of synovial fluid protein and expressed as nitric oxide; the result was then compared with clinical and arthroscopic findings of synovitis and cartilaginous degeneration. RESULTS: Significantly higher levels of nitric oxide (median, 0.331 micromol/mg) were seen in the patients with internal derangement and osteoarthritis than in the control group (median, 0.001 micromol/mg; P<.0001). Synovial fluid from joints with pain in the joint area had significantly higher levels of nitric oxide than did fluid from joints without such pain. Synovial fluid from joints with degenerative changes (median, 0.467 micromol/mg) had significantly higher levels of nitric oxide than did fluid from joints without osteoarthritis (median, 0.057 micromol/mg; P<.05). Although the levels of nitric oxide in synovial fluid aspirates were markedly elevated in some joints with synovitis, there was no correlation between the levels of nitric oxide and the presence of synovitis. CONCLUSIONS: The findings indicate that increased levels of nitric oxide are involved in the pathogenesis of cartilaginous degeneration of the temporomandibular joint.
A case of megalocornea-mental retardation syndrome complicated with bilateral sensorineural hearing impairment.
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Craniocervical junction synovial cyst associated with atlanto-axial dislocation--case report.
A 51-year-old female presented with a rare case of synovial cyst at the cruciate ligament of the odontoid process associated with atlanto-axial dislocation, manifesting as a history of headache and numbness in her left extremities for 5 months, and progressive motor weakness of her left leg. Neuroimaging studies revealed a small cystic lesion behind the dens, which severely compressed the upper cervical cord, and atlanto-axial dislocation. The cyst was successfully removed via the transcondylar approach. C-1 laminectomy and foramen magnum decompression were also performed. Posterior craniocervical fusion was carried out to stabilize the atlanto-axial dislocation. The cyst contained mucinous material. Histological examination detected synovial cells lining the fibrocartilaginous capsule. Synovial cysts of this region do not have typical symptoms or characteristic radiographic features. Careful preoperative evaluation of the symptoms and a less invasive strategy for removal of the cyst are recommended.
[A successful surgical case of giant arch aneurysm with severe pulmonary dysfunction and angina pectoris].
A 70-year-old female was admitted to our unit with chief complaints of dyspnea on effort and angina pectoris. She had suffered from chronic bronchitis. Chest CT scan demonstrated a giant arch aneurysm which strongly attached to the left anterior chest wall. Coronary angiogram showed two vessels disease. She successfully underwent coronary artery bypass grafting and total arch replacement under selective cerebral perfusion. She needed long respiratory care because of her pulmonary dysfunction. But she could wean from the ventilator under intensive respiratory care on 46th postoperative days and was discharged on foot.
47,XX,UPD(7)mat,+r(7)pat/46,XX,UPD(7)mat mosaicism in a girl with Silver-Russell syndrome (SRS): possible exclusion of the putative SRS gene from a 7p13-q11 region.
Maternal uniparental disomy for chromosome 7 (UPD7) may present with a characteristic phenotype reminiscent of Silver-Russell syndrome (SRS). Previous studies have suggested that approximately 10% of SRS patients have maternal UPD7. We describe a girl with a mos47,XX,+mar/46,XX karyotype associated with the features of SRS. Chromosome painting using a chromosome 7 specific probe pool showed that the small marker was a ring chromosome 7 (r(7)). PCR based microsatellite marker analysis of the patient detected only one maternal allele at each of 16 telomeric loci examined on chromosome 7, but showed both paternal and maternal alleles at four centromeric loci. Considering her mosaic karyotype composed ofdiploid cells and cells with partial trisomy for 7p13-q11, the allele types obtained at the telomeric loci may reflect the transmission of one maternal allele in duplicate, that is, maternal UPD7 (complete isodisomy or homodisomy 7), whereas those at the centromeric loci were consistent with biparental contribution to the trisomic region. It is most likely that the patient originated in a 46,XX,r(7) zygote, followed by duplication of the maternally derived whole chromosome 7 in an early mitosis, and subsequent loss of the paternally derived ring chromosome 7 in a subset of somatic cells. The cell with 46,XX,r(7) did not survive thereafter because of the monosomy for most of chromosome 7. If the putative SRS gene is imprinted, it can be ruled out from the 7p11-q11 region, because biparental alleles contribute to the region in our patient.
Effects of D2 dopamine receptor agonist and antagonist on brain activity in the rat assessed by functional magnetic resonance imaging.
The effects of D2 dopamine receptor agonist, bromocriptine (BROMO), and antagonist, haloperidol (HPD), on brain activity were investigated in rats by functional magnetic resonance imaging. T2*-weighted signal intensity was increased in the hypothalamus at 120 min after acute administration of BROMO, and in the ventral posterior and dorsomedial nuclei of the thalamus from 30 to 120 min. In contrast, the signal intensity was decreased in the caudate-putamen at 30 min after acute administration of HPD, in the hypothalamus from 30 to 60 min, and in the perirhinal cortex at 30 min. After chronic (2 weeks) HPD treatment, acute administration of HPD decreased signal intensity in the caudate-putamen at 60 min, in the hypothalamus at 30 min, the perirhinal cortex from 2 to 120 min, the dorsomedial and ventral posterior nuclei of the thalamus from 2 to 120 min, and the medial nucleus of the amygdala from 60 to 120 min. These results suggest that (1) the D2 receptor agonist increased the activity of the thalamic nuclei and the hypothalamus, while the D2 receptor antagonist suppressed brain activity in the regions where D2 receptors were present, (2) the suppression of brain activity in the thalamic nuclei and the perirhinal cortex by acute HPD administration was enhanced by chronic HPD treatment, and (3) the effects of antipsychotic drugs on the thalamus, amygdala, and perirhinal cortex may be related to their therapeutic efficacy, since clinical improvement in schizophrenic patients appears several days after the start of HPD treatment.
Hypothalamic control of amino acid appetite.
Preference for umami taste materials, such as monosodium L-glutamate (MSG) and the 5'-ribonucleotides, inosine 5'-monophosphate (IMP) and guanosine 5'-monophosphate (GMP), varies as a consequence of protein nutrition. Rats fed diets deficient in dietary protein or an essential L-amino acid (AA), L-lysine (Lys), avidly consumed Lys, glycine and NaCl but not umami substances. However, when the rats' protein nutrition was normal or when they were recovering from deficiency, a preference for umami substances was evident. These data suggest that the central mechanism for recognition of protein malnutrition may be coupled with umami taste preference. To test this, Lys-deficient and normal rats were employed as a model for taste preference changes. AA levels in plasma and brain remain essentially unchanged throughout the day while the rat is on standard chow but are altered during Lys deficiency. The recognition site for the deficit in the rats' brains was localized to the ventromedial (VMH) and lateral (LHA) hypothalamus as determined by functional magnetic resonance imaging (fMRI, 4.7 Telsa). Studies of single neuron activity in the LHA of Lys-deficient rats suggested that neuronal plasticity occurred. Following Lys deficiency, cells responded specifically to Lys, both iontophoretically applied and during ingestion of AA. Other LHA neurons of nondeficient rats differentially responded to MSG. The present results suggest that the LHA and probably the VMH play important roles in recognition of deficient nutrients. Neural plasticity of hypothalamic cells helps maintain AA homeostasis. Furthermore, a preference for umami substances may be an indicator that the organism (rat or human) is free of protein malnutrition.
Islet-cell hyperplasia causing hyperinsulinemic hypoglycemia in an adult.
We report a patient, a 23-year-old man, who had clinical and laboratory findings suggestive of insulinoma. Although imaging studies did not reveal any tumors in the pancreas, distal pancreatectomy was performed because the possibility of small insulinoma could not be completely excluded. Grossly, the surgically removed pancreas did not reveal any tumors. Microscopically, the pancreas exhibited islet cell hyperplasia and nesidioblastosis. To our knowledge, this is the first authentic reported case of islet-cell hyperplasia occurring in a Japanese adult.
New radiological finding by magnetic resonance imaging examination of the brain in Coffin-Lowry syndrome.
We used magnetic resonance imaging (MRI) to examine the brain of a typical Coffin-Lowry syndrome (CLS) patient. There were many small perivascular focal areas of hypointensity in the white matter on T1-weighted images, similar to those found in mucopolysaccharidosis or perivascular leukomalacia. However, these changes could not seen in another patient we examined. Both patients showed normal urinary mucopolysaccharide patterns with chromatographic analysis. The cause of the MRI result is not known, but it could have a heterogeneous origin, and this result could represent an important indication defining one type of CLS.