Biomedical subjects
Publications and source records attributed to N Doi.
We report a case of metastasis of a hepatocellular carcinoma to the bladder. Clinically the tumor was suspected to be a primary bladder tumor with subsequent metastasis to the liver. However, the pathological diagnosis yielded different results. The tumor cells resembled liver cells and sometimes bile production was even observed. No therapy was available and the patient died of cachexia 6 months later.
Amino acid metabolism in endogenous psychoses has been discussed in relation to monoamine synthesis. There are no consistent findings which prove altered monoamine syntheses to be the primary change. Our finding, which suggests decreased amino acid transport across the blood-brain barrier in schizophrenia, does not necessarily mean an insufficient amino acid supply to the brain. Several lines of investigation have shown the possibility of the involvement of glutamatergic dysfunction in the pathogenesis of schizophrenia. Our recent finding of decreased CSF asparagine concentration in schizophrenia and its positive correlation with the response to neuroleptics may support this hypothesis. Recently, free D-serine, an allosteric agonist on NMDA-receptor, has been reported to exist in the rat brain, suggesting that D-serine is an intrinsic ligand. The pathogeneses of endogenous psychoses might be studied in terms of disturbed metabolism of amino acid, as allosteric regulater of neuro-receptor, as well as neurotransmitter and precursor of monoamines.
A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
The effects of glucocorticoids on rat hippocampal CA1 pyramidal neurons were studied using brain slice preparations. At 10 days after bilateral adrenalectomy, a localized region of CA1 showed a drastic reduction of excitability induced by CA3 stimulation as compared to control. The region of CA1 most effected was 1.4-2.0 mm from the most rostral side of the hippocampus. Upon perfusion of corticosterone, the response to synaptic activation was reduced in this region in slices from adrenalatomized animals increased rapidly toward control values, volatile responses in other regions were unaffected. These results suggest that glucocorticoid receptors are concentrated in restricted regions of hippocampus and that these receptors have important roles in regulation of synaptic excitability.
Using rat hippocampus we have studied the pattern of neuronal death, abnormal discharge and loss of electrical excitability in slices prepared from animals subjected to bilateral, four-vessel cerebral anoxia and in slices prepared from normal animals that are subjected to anoxia in the recording chamber. As others have reported, pyramidal neurons in area CA1 are lost first after anoxia, while CA3 neurons have an intermediate sensitivity, and those in dentate are relatively anoxia-resistant. After anoxic damage to the intact animal, neurons in both CA1 and CA3 show abnormal bursting discharges in response to synaptic activation for several days, and then the response in CA1 decreases in amplitude and finally the area become unexcitable. While antagonists for N-methyl-D-aspartate (NMDA) receptors have essentially no effect on synaptic responses in control animals, they reduce the bursting responses and greatly depress the small responses in CA1 as neurons are becoming unexcitable after anoxia. With intracellular recording CA1 neurons from animals made transiently anoxic, in contrast to controls, show prolonged synaptic responses, the later components of which are blocked by NMDA antagonists. When slices from normal animals are subjected to anoxia such that excitability is totally lost over a period of about 10 min, there is no significant membrane depolarization during the anoxic episode and recovery of excitability occurs with reoxygenation. However, a period of hyperexcitability and bursting follows and electrical excitability is lost in CA1 but not CA3 neurons after about 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)
The binding sites of lectins in parathyroid glands were determined by an immunohistochemical method in normal parathyroid gland, hyperplasia, adenoma and carcinoma, the used lectins were commercially available Glycine max (SBA), Concanavalin enciformis (Con A), Triticum vulgaris (WGA), Richinus communis (RCA), Banderiaea simplicifolia II (BSA II) and Arachis hypogaea (PNA). For normal parathyroid glands (2 cases) and hyperplasia (2 cases), WGA and BSA II were stained in cytoplasma and cell membrane. For carcinoma (1 cases), all lectins but BSA II were positively stained. In particular, SBA revealed more stronger stain than any other hystological types. From the staining patterns of lectins, it was suggested that adenomas (22 cases) be divided into one group similar to carcinoma and the others to normal parathyroid gland and hyperplasia. But there was no difference in clinical data of patients between the two groups.
1. The effects of baclofen and GABA on rat piriform cortex neurons were investigated electrophysiologically using a brain slice preparation. 2. At resting potential GABA depolarized and baclofen hyperpolarized the cell, probably through activation of Cl and K conductances acting at GABAA and GABAB receptors, respectively. 3. The GABAA receptors were concentrated on the apical and basal dendrites near the cell body, while the baclofen-sensitive GABA receptors were concentrated particularly on the basal dendrites. 4. The different distributions of receptor localization must have functional consequences which remain to be elucidated.
Last year, we reported that human papilloma virus type 16 genome (HPV 16 genome) was detected in a case (S.Y.) of bladder carcinoma in situ (bladder CIS) (Cancer Res., 1988). Since then, a number of bladder tumors other than CIS were searched for HPV genome. However, no HPV genome was detected in the bladder tumors. From the results, we consider that HPV may not have a relation with all types of bladder tumor but with only a part of it. In the current report, the case (S.Y.) is presented more precisely than before, in particular on the characteristic bladder lesion. The patient was a 40-year-old female with immunodeficiency and anemia who was referred from a hospital with a complaint of asymptomatic pyuria. Cystoscopic examination revealed a bladder tumor, well-demarcated, white and velvety lesion with slight elevation. On November 25, 1987, she underwent total cystectomy, resection of the anterior vaginal wall and of a part of vulval skin, and ileal conduit formation. Postoperative course was stormy because of bleeding from the wounds and thrombophlebitis in the right femoral vein. In spite of the episodes, she eventually recovered and was discharged 2 months later. However she was readmitted 9 months later due to severe anemia which was ascribed to acute myelogenous leukemia. She is now on cancer chemotherapy for leukemia.
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Reports seeking the rate of successful echography of the fetal scrotum, penis and labia majora classified by individual weeks of gestation over the long period from the 22nd to the 41st week of gestation, are few. In the present study, the rates of successful echography of the scrotum, penis, labia majora, M-type and F-type of the fetal APG region in the breech and transverse presentations in each week of gestation for the period from the 22nd to the 41st week of gestation were pursued with a view to finding out the best suited time for the observation of each image. Ultrasonography was performed 3039 times in total on 620 pregnant women who delivered their babies, and the following results were obtained: The rates of successful echography classified by presentation decreased in the order of cephalic, breech and transverse presentations. The rates of successful echography with the first and second manipulations classified by individual weeks of gestation were also determined, and the optimal periods for observation were sought. The rates of correct echography as a whole were also determined, with the following results: Breech presentation is 74.1% in male fetuses and 68.3% in female fetuses; Transverse presentation is 66.2% in male fetuses and 58.6% in female fetuses, respectively.
Continuous monitoring of the intracranial pressure and ventricular infusion test were carried out in 13 cases in which normal pressure hydrocephalus (NPH) was suspected. The infusion test was performed by intraventricular bolus injection of 8 ml of saline. The result was collated with the effect of shunting operation, which was judged by means of the improvement in the clinical symptoms and the amplitude of contingent negative variation. The excellent effect of shunting operation was obtained in the patients who showed the T of more than 200 sec, the compliance of less than 1.0 ml/mmHg, the conductance to outflow of less than 0.8 ml/mmHg/min and CSF outflow resistance of more than 15 mmHg/ml/min. In 3 cases out of the 5 effective cases, A or B wave was seen. However, appreciable variation of the values was shown among the cases so that it was concluded that the all-round-consideration must be done to select the case for the shunting operation with the findings in RI-cisternography, pneumoencephalography, computerized tomography and so on. This fact might indicate the existence of the complicated pathophysiology in NPH resulted from not only the impairment of cerebrospinal fluid circulation but also the disturbance of cerebral blood flow, changes in plasticity of the brain and so on.
The distribution of membrane-bound monoamine oxidase in 30 strains of various bacteria was studied. Monoamine oxidase was determined by using an ammonia-selective electrode; analyses were sensitive and easy to perform. The enzyme was found in some strains of the family Enterobacteriaceae, such as Klebsiella, Enterobacter, Escherichia, Salmonella, Serratia, and Proteus. Among strains of other families of bacteria tested, only Pseudomonas aeruginosa IFO 3901, Micrococcus luteus IFO 12708, and Brevibacterium ammoniagenes IAM 1641 had monoamine oxidase activity. In all of these bacteria except B. ammoniagenes, monoamine oxidase was induced by tyramine and was highly specific for tyramine, octopamine, dopamine, and norepinephrine. The enzyme in two strains oxidized histamine or benzylamine. Correlations between the distributions of membrane-bound monoamine oxidase and arylsulfatase synthesized in the presence of tyramine were discussed.
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Some properties and the intracellular distriubtion of inorganic pyrophosphatase in rabbit dental pulp were determined. This enzyme was sensitive to Mg2+, and not inhibited by imidazol and CN- which are inhibitors of alkaline phosphatase. Inorganic pyrophosphatase was found predominantly in the supernatant fraction.
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To examine in more detail the peripheral visual field loss after macular hole surgery, we reviewed a series of 38 consecutive patients (44 eyes) with idiopathic macular hole who underwent vitrectomy and fluid-gas exchange. Ten (22.7%) eyes of 9 patients developed peripheral visual field loss shortly after successful surgery. This complication was characterized by mild to moderate wedge-shaped visual field loss that predominantly affected the inferotemporal periphery. Of these 9 patients, 2 complained of peripheral visual field loss, and the 7 others remained asymptomatic. The peripheral visual field loss remained unchanged for a mean follow-up of 18.5 months, except in one case of complete recovery. The thickness of the retinal nerve fiber layer was measured postoperatively to determine whether any damage to the optic nerve head had occurred during surgery. The information obtained in this study did not provide conclusive evidence for the understanding of the pathomechanism of the macular hole surgery-associated visual field loss. Peripheral visual field defect after otherwise uneventful surgery for idiopathic macular hole is probably not uncommon. This complication is variable in its severity and is usually permanent. Whether it is caused by any surgical trauma to the optic nerve head remains to be elucidated.
PURPOSE: To further understand postoperative complications after vortex vein damage during scleral buckling surgery. METHODS: The records of 34 patients (34 eyes) with vortex vein damage during scleral buckling surgery for rhegmatogenous retinal detachment were reviewed and compared with the records of 410 eyes undergoing similar surgery without vortex vein damage. RESULTS: Postoperative complications were noted in 16 eyes (47%) of the damaged vortex vein group. The incidence of choroidal detachment, vitreous opacities, intraocular pressure elevation, and vitreous hemorrhage were 27%, 18%, 9%, and 6%, respectively, with a higher incidence than in the group without vortex vein damage. Other complications included development of epiretinal membrane (9%), subretinal hemorrhage (3%), and anterior segment ischemia (3%). Serous choroidal detachment occurred in the early postoperative days and subsided within 3 weeks. Vitreous opacification became marked in the later periods and continued for 2 months or longer. The incidence of postoperative choroidal detachment in the vortex vein damage group was related to the patient's age (P = .002) and the cutting of the vortex veins (P = .048), but was not related to preoperative conditions of retinal detachment or the number of vortex veins damaged. All the eyes except one achieved retinal reattachment after initial surgery. CONCLUSIONS: Choroidal detachment and vitreous opacity are common after scleral buckling surgery with vortex vein damage. Although intervention of the vortex veins during scleral buckling surgery is acceptable when performing otherwise difficult to achieve ample scleral indentation, it should be minimized to avoid increased incidence of postoperative complications.