Biomedical subjects
Publications and source records attributed to T Inagaki.
PURPOSE: We report on a case of prostatic cancer with multiple bone metastases, including right orbital involvement. METHODS/RESULTS: Hormonal treatment and local irradiation to the right orbit were performed. Subjective symptoms with exophthalmos and pain disappeared. CONCLUSIONS: We report on a case of prostatic cancer metastasizing to the right orbital bone.
The Eisai hyperbilirubinemic rat (EHBR) is a Sprague-Dawley rat (SDR) mutant with conjugated hyperbilirubinemia as an autosomal recessive trait. EHBRs manifest jaundice from birth, which is permanent except for a transient decrease at 6-8 weeks of age. To investigate whether the hyperbilirubinemia affects pancreatic exocrine function and acinar cell growth, EHBRs at 6 (without jaundice) and 12 weeks (with jaundice) of age were compared, along with SDRs as controls. Pancreatic wet weights did not significantly differ, but amylase content of acini was lower in EHBRs than SDRs. No correlation was found between pancreatic wet weight and serum bilirubin levels in EHBRs. In vitro amylase release in response to 1-100 pM cholecystokinin octapeptide (CCK-8), 1 microM 12-O-tetradecanoylphorbol 13-acetate, and 2.5 microM calcium ionophore A23187, and in vivo pancreatic secretion stimulated by CCK-8 (0.08 microg/kg body weight/h) were significantly lower in the EHBR cases than in the SDRs. At the electron microscopic level, many acinar cell nuclei were pyknotic, most elements of their Golgi complexes were atrophied, some mitochondria demonstrated fusion, and the rough-surfaced endoplasmic reticulum (RER) was dilated in EHBRs. These findings are indicative of a hypofunctional state. However, no differences between EHBRs at 6 and 12 weeks of age were evident, suggesting that the hyperbilirubinemia does not exert any pronounced influence on acinar cell growth or pancreatic exocrine function.
Striatal dopamine contents in C57BL/6J mice were reduced at 24 h after intracerebroventricular (ICV) administration of 1-methyl-4-phenyl-1,2, 3,6-tetrahydropyridine (MPTP) or 1-methyl-4-phenylpyridinium (MPP+) in a dose-dependent manner. A dose of 1.8 microg MPP+ significantly (P < 0.05) suppressed the dopamine contents, whereas a similar dose of MPTP did not. A definite positive correlation between urinary contents of alpha1-microglobulin (alpha1M) and ulinastatin (UT) existed in normal mice. However, this correlation was nullified by ICV administration of 18 and 36 microg MPTP or 1.8 and 18 microg MPP+. With 1.8 microg MPTP, a positive correlation between urinary contents of alpha1M and UT was displayed. The urine volume, creatinine content, glomerular filtration rate, alpha1M and UT contents, and alpha1M/UT ratio of urine collected for 24 h post-ICV administration of MPTP or MPP+, were not statistically different from those of control mice. Our findings suggest that the central effects of MPP+, a neurotoxic metabolite of MPTP, nullify the positive correlation between urinary contents of alpha1M and UT without affecting renal functions.
In the previous study [Takeda et al. (1996) Neurosci Lett 221: 17-21], we reported that the advanced glycation end products (AGEs) in the external space of neuronal perikarya (extraneuroperikaryal AGE deposits) were significantly abundant in the Alzheimer's brain. In this study, we investigated the spatial relationship of the extraneuroperikaryal AGE (carboxymethyllysine and pentosidine) deposits in astrocytes and microglial cells in the Alzheimer's disease brain using double immunolabelling for AGEs and astrocyte or microglial cell markers. Most of the extraneuroperikaryal AGE deposits were co-localized with glial fibrillary acidic protein-positive astrocytes. AGE deposit-bearing astrocytes also contained Gomori-positive granules. Furthermore, some of the extraneuroperikaryal AGE deposits were co-localized with microglial cells. These extraneuroperikaryal AGEs may activate astrocyte and microglia, and play a role in pathogenesis of Alzheimer's disease.
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BACKGROUND: Several reports in the 1970s suggested that etidronate disodium might be clinically useful to prevent calcium stones, but the use of etidronate in the urolithiasis field was discontinued due to adverse effects of this drug on skeletal turnover and mineralization. Because the drug might affect not only crystallization, but also crystal-tubular interactions, we investigated the minimum dose of etidronate necessary to effectively prevent stone recurrence without adverse side effects. METHODS: We examined the effect of etidronate on the crystallization of calcium oxalate, calcium phosphate and magnesium ammonium phosphate using synthetic urine and measured by an aggregometer. We also studied its effect on the adhesion of calcium oxalate monohydrate crystals to Madin-Darby canine kidney (MDCK) cells in vitro. RESULTS: Etidronate affected the crystallization+ of not only calcium phosphate and calcium oxalate, but also magnesium ammonium phosphate in synthetic urine. The inhibitory activities on these crystallizations were detected at extremely low drug concentrations. Etidronate also had a strong inhibitory activity against the adhesion of calcium oxalate crystals to MDCK cells. CONCLUSION: Although further studies are necessary regarding the effects of etidronate on crystallization and crystal adhesion both in vivo and in vitro, and the appropriate schedule of dosing to prevent side effects, it is possible that etidronate may be useful in the treatment of urinary stones.
Hypersomnia occurs frequently in patients with myotonic dystrophy (MyD). We performed a quantitative immunohistochemical study of serotonin (5-HT)-containing neurons linked to hypersomnia in the dorsal raphe nucleus (DRN) and the superior central nucleus (SCN) in 8 patients with MyD, 5 of whom showed hypersomnia, and in 12 age-matched controls. The densities of 5-HT neurons in the DRN and the SCN were significantly lower in MyD patients with hypersomnia than in MyD patients without hypersomnia and controls. These data suggest that the loss of 5-HT neurons of the DRN and the SCN is associated with the presence of hypersomnia in MyD.
OBJECTIVE: To clarify the possible relation between the extent of involvement of catecholaminergic neurons and the presence of alveolar hypoventilation in patients with myotonic dystrophy (MyD). BACKGROUND: Respiratory insufficiency has been reported frequently in MyD patients. Recent data support the hypothesis that this respiratory failure results from a primary dysfunction of the CNS. METHODS: The authors performed a quantitative immunoreactive study of tyrosine hydroxylase immunoreactive (TH+) neurons linked to hypoventilation in the dorsal central medullary nucleus (DCMN), the ventral central medullary nucleus (VCMN), and the subtrigeminal medullary nucleus (SMN)--where the autonomic respiratory center is thought to be located--in eight MyD patients and in 10 age-matched control subjects. Alveolar hypoventilation of the central type was present in three of the MyD patients but not in the remaining MyD patients or the control subjects. RESULTS: The densities of TH+ neurons of the DCMN, the VCMN, and the SMN in MyD patients with hypoventilation were significantly lower than in those without hypoventilation (p < 0.02, p < 0.01, and p < 0.01, respectively) and control subjects (p < 0.01, p < 0.01, and p < 0.01, respectively). CONCLUSIONS: These data suggest that the loss of TH+ neurons of the DCMN, the VCMN, and the SMN is associated with the presence of hypoventilation in MyD and may be an important feature of MyD.
We present a case of asynchronous development of transitional cell carcinoma in urinary bladder and renal pelvis after prolonged cyclophosphamide therapy. A 57-year-old woman had received 290 g cyclophosphamide for 13 years because of therapy for non-Hodgkin lymphoma. She was suffered from dysuria and macrohematuria and visited our clinic. Cystoscopy, CT and MRI revealed invasive bladder tumor and total cystectomy was performed. Histological diagnosis was transitional cell carcinoma, G3 < G2, pT4. Six months after the cystectomy, a follow up urography and computerized tomography showed left renal pelvic tumor. The patient underwent total nephroureterectomy, and the histological diagnosis was transitional cell carcinoma, G3, pT3. We reviewed cyclophosphamide induced urothelial carcinomas from Japanese and world literatures.
A novel isochroman carboxylic acid CJ-12,373 was isolated from Penicillium sp. CL22557. CJ-12,373 inhibits both DNA gyrase-mediated supercoiling and relaxation without the formation of a cleavage intermediate, suggesting that CJ-12,373 inhibits DNA gyrase at a stage distinct from the religation step. CJ-12,373 is not selective for procaryotic DNA gyrase as it also inhibits relaxation mediated by eukaryotic topoisomerase II. The antimicrobial potency of CJ-12,373, however, is largely attributed to its inhibition of DNA gyrase.
Among methods of controlling hypercholesterolemia and hyperlipidemia is the direct stimulation of hepatic low density lipoprotein (LDL) receptors. Two novel lactone compounds, CJ-12,950 and CJ-13,357, containing and unusual oxime moiety, were isolated from a zygomycete Mortierella verticillata. These lactones are potent inducers of the LDL receptor gene in vitro, that enhanced LDL receptor expression in human hepatocytes 2-fold at 100 nM.
Eight novel quinolones with anti-Helicobacter pylori activity were isolated from the actinomycete Pseudonocardia sp. CL38489. The quinolones were very potent against H. pylori with MICs up to 0.1 ng/ml. The quinolones appear to be specific for H. pylori, since they did not show antimicrobial activity when tested against a panel of other microorganisms.
A kappa opioid receptor binding inhibitor was isolated from the fermentation broth of a basidiomycete, Hericium ramosum CL24240 and identified as erinacine E (1). Three analogs of 1 were produced by fermentation in other media and by microbial biotransformation. Of these compounds, 1 was shown to be the most potent binding inhibitor. Preliminary SAR studies of these compounds indicated that all functional groups and side chains were required for the activity. Compound 1 was a highly-selective binding inhibitor for the kappa opioid receptor: 0.8 microM (IC50) for kappa, >200 microM for mu, and >200 microM for delta opioid receptor. Compound 1 suppressed electrically-stimulated twitch responses of rabbit vas deferens with an ED50 of 14 microM. The suppression was recovered by adding a selective kappa opioid receptor antagonist nor-binaltorphimine, indicating that 1 is a kappa opioid receptor agonist.
A 62-year-old man developed clumsiness, vertical ophthalmoplegia, right-side dominant parkinsonism, pyramidal signs, limb-kinetic apraxia and dementia. His brain MRI and SPECT revealed mild fronto-parietal atrophy and hypoperfusion predominately on the right side. At the age of 65, the patient died of sepsis. The duration of his illness was approximately 3 years. Clinical diagnosis was corticobasal degeneration (CBD). On neuropathological examination, there was no neuronal loss and many neurofibrillary tangles (NFTs) in the cerebral cortices. Basal ganglia and substantia nigra showed moderate to severe neuronal loss. And there were many NFTs and argyrophillic threads (threads) in the subthalamic nucleus and nuclei of the brainstem. These findings were almost compatible to those of PSP. However, the following findings were atypical for PSP, 1) mild atrophy and absence of gliosis in the tegmentum of the brain stem, 2) Mild neuronal loss in the subthalamic nucleus and the dentate nucleus without grumose degeneration. Furthermore, characteristic findings were noted on modified Gallyas-Braak stain. Numerous threads and many astrocytic plaques (AP) were shown in cerebral cortices, which were particular to CBD cases. So this case demonstrated neuropathological findings of both PSP and CBD. Therefore, it was difficult to classify this case as either PSP or CBD, and we diagnosed this case as a neuropathological overlapping case of both PSP and CBD.
Although prostate-specific antigen (PSA) is a valuable marker of prostate cancer, some untreated patients with advanced prostate cancer have normal PSA values. Over a period of 5 years, we reviewed pretreatment serum PSA levels in 131 patients with advanced prostate cancer (stages C and D). Ten patients (7.6%) had normal PSA values. The histological type of prostate cancer associated with normal PSA values was variable and the prognosis was not so poor. Immunostaining for PSA was performed on the resected prostate tissue of the 10 patients. PSA staining was positive in 5 cases, negative in 3 cases, and equivocal in the remaining 2 cases. In conclusion, PSA is not always useful, especially for following patients with normal PSA values.
The purpose of this investigation was to study the indication of cerebral angiography in recent operations for cerebral aneurysms. Cerebral angiography has been used for diagnoses and operations for cerebral aneurysms, but, as the diagnostic procedures such as magnetic resonance angiography (MRA) and three dimensional computed tomographic angiography (3D-CTA) have made remarkable progress, cerebral angiography is not always an indispensable diagnostic tool for cerebral aneurysm operations. One hundred nineteen patients (including 40 patients with ruptured aneurysms) out of 165 patients (including 61 patients with ruptured aneurysms) were diagnosed and operated on following MRA and 3D-CTA. All of these cases of cerebral aneurysms were operated uneventfully without the need for cerebral angiography. We concluded that cerebral angiography is not needed for diagnoses and operations of small common cerebral aneurysms such as middle cerebral artery aneurysms, internal carotid artery-posterior communicating artery aneurysms and anterior communicating artery aneurysms. Cerebral angiography is necessary only in relatively large aneurysms to confirm the dynamic circulation of the cerebral blood flow before operation.
A case of diploic epidermoid in the right parietal bone was presented. A 66-year-old male was admitted to our hospital because of aphasia. Plain skull radiogram showed an osteolytic lesion in the right parietal bone. Computed tomography revealed a mass with destruction of the parietal bone extending from an inner to an outer table. The mass was shown by MR imaging as hypointensity on the T1-weighted image and as hyperintensity on the T2-weighted image. The hyperintensity became more remarkable by using a diffusion technique. Based on these findings, a preoperative diagnosis of right parietal epidermoid was made. The mass was totally removed and diagnosed pathologically as epidermoid. It was concluded that diploic epidermoid invading intradurally could be differentiated from other osteolytic tumors by using MR diffusion-weighted image.
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