Biomedical subjects

J Satoh

Publications and source records attributed to J Satoh.

At least 109 records · Page 6Linked to original sources

PubMed1994

The colonic neobladder: a stoma-free bladder substitute after radical cystectomy--preliminary results in six patients.

We have used a urethral colonic pouch for total bladder replacement in 6 bladder cancer patients after radical cystectomy. The distal ileum, cecum, ascending colon and the right third of the transverse colon were isolated. The cecum and colon were opened along the tenia and a detubulized pouch was created. The ureters were sutured to the terminal ileum. The maximum pressure wave measured ranged 22-58 cmH2O, and the amount of residual urine varied between 0 and 58 ml. All patients were completely continent during the day and slight incontinence at night was observed in 3. By amputating the right colonic artery, the pouch is easily moved to the urethral stump and serves as a low pressure neobladder after cystoprostatectomy.

Adult↗

PubMed1994

A case of posttherapeutic sclerotic change of bone metastasis from renal cell carcinoma which proved histopathologically to be complete response.

A 60-year-old man with renal cell carcinoma and metastases to the right 7th rib and L2 vertebra (T2N0M1, OSS) was treated with interferon-alpha and the uracil and tegafur combination following nephrectomy. One and a half years later on bone scintigraphy, the abnormal accumulation had disappeared at the L2 vertebra and weakened in its intensity at the right 7th rib. Plain X-ray revealed that the metastatic lesion at the right 7th rib had decreased in size and had been replaced by calcification. The right 7th rib was removed surgically and step-sectioned pathological specimens revealed necrosis with no viable cancer cells.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1994

[Membranous and penile urethral involvement in bladder cancer patients-- review of cystoprostatourethrectomy specimens].

We studied 18 cystoprostatourethrectomy specimens, which were surgically removed for bladder cancer and step-sectioned in 0.5 cm thickness, to evaluate the relationship of the membranous and penile urethral lesions, with the multiplicity of bladder cancer, association of carcinoma in situ (CIS), bladder neck involvement, and prostatic involvement. Thirteen cases were associated with CIS. There were four solitary bladder cancers and 14 were with multiple cancers. Twelve cases were with bladder neck involvement and seven with prostatic involvement. There were five cases of urethral involvement; two cases of CIS and three with dysplasia. No macroscopic urethral cancers were detected in the urethra. Four of the five cases of urethral involvement had multiple cancers with CIS and were associated with bladder neck and prostatic involvement. One case of urethral dysplasia had solitary bladder cancer and neither bladder neck nor prostatic involvement were observed. Statistical analysis revealed that prostatic involvement was the only significant risk factor for urethral involvement. Our study shows that bladder cancer patients with prostatic involvement should be excluded from the candidates for bladder substitution utilizing the retained urethra. When a neobladder is indicated to bladder cancer patients, each case should be followed carefully for urethral recurrence.

Adult↗

PubMed1994

[Heat shock proteins and neurological disorders].

Heat shock proteins (HSPs) are a highly conserved group of proteins which are produced when cells are confronted with a variety of stressful insults such as heat shock, hypoxia/ischemia, metabolic disruption, and exposure to cytotoxic reagents. Under unstressed conditions, HSPs act as molecular chaperones which play pivotal roles in the course of maturation of various cellular proteins. Under stressed conditions, they play a protective role against irreversible cell damage and promote recovery of the cells experiencing stress. In the central nervous system, proteins of the HSP 90, HSP 70, HSP 60, and small HSP families are expressed constitutively and/or induced by stressful events, differentially in distinct cell types. Aberrant expression of HSPs might be implicated in the pathogenesis of neurological disorders such as multiple sclerosis and Alzheimer's disease.

Heat-Shock Proteins↗

PubMed1994

[Penetration of the esophageal and gastric ulcers to the cardioaortic system following hiatus hernia: a lethal complication in the severely-handicapped].

Among the severely-handicapped, hiatus hernia (HH) and/or gastroesophageal regurgitation (GER) are not uncommon. We report here three patients with HH and/or GER. Two of them died of massive hemorrhage in the alimentary tract from the heart or the thoracic aorta due to penetration of the gastric or esophageal ulcer. The third patient died of pneumonia, but autopsy proved multiple esophageal ulcers, one of which reached the wall of the brachiocephalic artery without penetration. We propose that proper treatment for HH and/or GER is required for the severely-handicapped, including surgical intervention, before their general conditions become worse and decompensatory.

Adult↗

PubMed1993

Midkine that promotes survival of fetal human neurons is produced by fetal human astrocytes in culture.

Midkine (MK), a retinoic acid responsive gene product, is a novel heparin-binding growth factor with an apparent molecular weight of 14-kDa. In fetal human neuron cultures, addition of recombinant human MK (10-100 ng/ml) resulted in a 3-fold increase in the number of surviving neurons under the serum-free culture condition. Production of MK was identified in the conditioned medium of astrocyte-enriched cultures by immunoblotting but not in the medium of neuron-enriched cultures. The level of MK production was not affected by treatment with retinoic acid. These results indicate that in the developing human central nervous system, astrocytes secrete MK that exhibits potent trophic activity to neurons.

Animals↗

PubMed1993

Prevention of type I diabetes with lymphotoxin in BB rats.

We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). Recently we have further reported that lymphotoxin (LT), a cytokine with functional and structural characteristics similar to those of TNF, also protected NOD mice from diabetes. In this study, we have extended our observation on the LT to BB rats. Male and female BB/Wor rats were treated intraperitoneally with recombinant human LT three times a week from 4 to 11 weeks of age. The cumulative incidence of diabetes by 14 weeks of age was 24/30 (80.0%) in nontreated control rats, whereas it was 10/26 (38.5% vs control, P < 0.01) and 4/29 (13.8% vs control, P < 0.0001) in the rats treated with 1 x 10(3) and 1 x 10(4) of LT, respectively. There was no significant difference in nonfasting blood glucose levels and body weights between nontreated control and LT-treated rats, which were nondiabetic. In the LT-treated rats, intensity of insulitis was significantly reduced in comparison with the nontreated rats. Concanavalin A-stimulated TNF/LT productivity of spleen cells was significantly lower in BB/Wor and BB/Sendai rats than in Wistar rats or other normal rat strains. On the other hand, there was no difference between BB/Sendai and Wistar rats in the in vivo TNF/LT productivity induced with LPS or with IFN-gamma plus LPS, and the TNF/LT productivity of these rats was lower on stimulation with LPS alone, but higher with IFN-gamma plus LPS than the other normal rats. These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT.

Animals↗

PubMed1993

Prevention of autoimmune diabetes with lymphotoxin in NOD mice.

We have reported previously that chronic and systemic administration of a streptococcal preparation (OK-432), an inducer of TNF, or of recombinant hTNF prevented the development of IDDM in the two animal models of IDDM-NOD mice and BB rats. In this study, we examined the effect of LT, which is structurally and functionally related to TNF, on NOD mice with diabetes. The cumulative incidence of diabetes at 30 wk of age was 22 of 40 (55%) in nontreated female NOD mice and was 4 of 8 (50%; NS), 3 of 29 (10%; P < 0.001), and 0 of 8 (0%; P < 0.001) in female mice treated three times a week from 4 to 30 wk of age with 5, 50, or 500 U of recombinant hLT, respectively. Intensity of insulitis was slightly reduced in the long-term LT-treated mice. LT productivity by ConA-stimulated spleen cells was examined in vitro. Although no significant difference was found between NOD mice and the other mouse strains, female NOD mice were slightly but significantly (P < 0.01) lower producers of LT immunoreactivity than male NOD mice, the diabetes incidence of which is lower than that of females. The SMLR as a marker of normal immune response, which was reported to be impaired in autoimmune animals including NOD mice, was significantly lower in female than male NOD mice. However, the low SMLR in female NOD mice was significantly increased by the administration of LT, and the increase was mediated by the responder cells of the LT-treated mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Severe flare-up in a prostate cancer patient treated with luteinizing hormone-releasing hormone analogue depot.

A 65-year-old man with advanced prostate cancer was treated with a luteinizing hormone-releasing hormone (LH-RH) analogue. Four days after the initial injection of 3.6 mg of goserelin acetate, severe dyspnea developed due to worsening pleuritis carcinomatosa, which was considered as a flare-up. Chest drainage was required to save his life. Therefore, we emphasize the importance of treatment to prevent tumor flare during LH-RH analogue therapy.

Adenocarcinoma↗

PubMed1992

Constitutive expression of 65-kDa heat shock protein (HSP65)-like immunoreactivity in cultured mouse oligodendrocytes.

The expression of mycobacterial 65-kDa heat shock protein (HSP65)-like immunoreactivity in cultured mouse oligodendrocytes and astrocytes was investigated using three monoclonal antibodies (ML30, IA1, 3A) specific for the mycobacterial HSP65. In western blot analysis, these antibodies recognized the proteins with molecular weights approximately of 50-, 60-, and 70-kDa expressed in both heat-stressed and unstressed glial cells. When the cells were exposed to heat stress, the expression of both 50- and 70-kDa proteins was attenuated, whereas that of the 60-kDa protein was not affected. On immunocytochemical studies, an appreciable level of HSP65 immunolabelling was identified in most (> 90%) oligodendrocytes under both heat-stressed and unstressed conditions but only marginally detectable in most (> 95%) astrocytes. These results indicate that mouse oligodendrocytes in vitro express the mycobacterial HSP65-like immunoreactivity constitutively.

Animals↗

PubMed1992

Heterogeneous induction of 72-kDa heat shock protein (HSP72) in cultured mouse oligodendrocytes and astrocytes.

The expression of 72-kDa heat shock protein (HSP72) in cultured mouse oligodendrocytes and astrocytes exposed to heat shock was investigated by double immunolabelling with anti-HSP72 monoclonal antibody (C92F3B-1) and antibodies against galactocerebroside (GalC) or glial fibrillary acidic protein (GFAP). After 3 h recovery from heat shock, an intermediate level of HSP72 immunolabelling was localized in the nucleolus and cytoplasm of astrocytes (less than 25%) and to a lesser extent in oligodendrocytes (less than 2%). After 8-48 h, HSP72 was expressed intensely in the cytoplasm and nuclear matrix of oligodendrocytes (20-40%), while weak/intermediate immunostaining was detectable in astrocytes (5-15%). The levels of HSP72 expressed in oligodendrocytes and astrocytes decreased around 72-120 h, but a few oligodendrocytes (4%) remained intensely immunolabelled. These results indicate that heat shock induces HSP72 in both oligodendrocytes and astrocytes. However, this response is heterogeneous.

Animals↗

PubMed1992

Coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in mouse clonal hybrid neurons derived from the septal region.

Two clonal immortalized neurons designated SN6.1b and SN6.2a were isolated by limiting dilution from a mouse embryonic septal cholinergic neuronal hybrid cell line SN6 (Hammond et al., 1986). In the serum-containing medium without extra differentiating agents, one-third of SN6.1b cells stably exhibited a morphology of differentiated neurons with extensive elaborate neurites, while a majority of SN6.2a cells, along with the parent cell line SN6, were round in shape with poorly branched short processes. Neurochemical studies showed that both clones synthesized choline acetyltransferase (ChAT), dopamine, norepinephrine, serotonin, and glutamate. Immunocytochemically, they expressed a number of neuronal antigens, such as 200-kDa neurofilament protein, neuron-specific enolase, microtubule-associated protein 2, tau protein, tubulin, neural cell adhesion molecule, Thy-1.2, saxitoxin-binding sodium channel protein, ChAT, tyrosine hydroxylase, serotonin, and glutamate. The coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in the clonal hybrid septal neurons that express a variety of immunocytochemical properties of differentiated neurons suggests that embryonic septal cholinergic neurons are potentially multiphenotypic with respect to neurotransmitter synthesis.

Amino Acids↗

PubMed1992

Establishment of mouse-immortalized hybrid clones expressing characteristics of differentiated neurons derived from the cerebellar and brain stem regions.

Two clonal immortalized neurons designated CL8c4.7 and CL8a5.2 were established by somatic cell fusion between a hypoxanthine phosphoribosyltransferase-(HPRT-) deficient neuroblastoma N18TG2 and newborn mouse cerebellar/brain stem neurons. In the serum-containing medium without extra differentiating agents, both clones exhibited a morphology of differentiated neurons. They contained high levels of glutamate but no gamma-aminobutyric acid (GABA). The CL8a5.2 clone synthesized choline acetyltransferase and serotonin. In immunocytochemical studies, both clones expressed 200 kD neurofilament protein, neuron-specific enolase, microtubule-associated protein 2 (MAP2), tau protein, neuronal cell adhesion molecule (N-CAM), HNK-1, Thy-1.2, saxitoxin-binding sodium channel protein, and glutamate. Synaptophysin immunoreactivity was identified in the neuritic terminals of CL8c4.7 cells. Most of these antigens were barely detectable on N18TG2 cells. Electrophysiologically, both clones generated action potentials in response to electrical stimuli. The hybrid clones that express characteristics of differentiated neurons derived from the cerebellar and brain stem regions might be invaluable for the study of the molecular basis of neuronal differentiation and degeneration in these regions.

Amino Acids↗

PubMed1992

Immunocytochemical and ultrastructural studies of neuronal and oligodendroglial cytoplasmic inclusions in multiple system atrophy. 2. Oligodendroglial cytoplasmic inclusions.

Oligodendroglial cytoplasmic inclusions (OCI) in multiple system atrophy were investigated immunocytochemically and ultrastructurally. Among the 17 cases examined, 16 had OCIs. Almost all OCIs were positive for both alpha B-crystallin and ubiquitin. The antibodies against tubulin, paired helical filament and tau stained OCIs to various extents. Ultrastructurally OCIs consisted of meshworks of granule-associated filaments about 25 nm in diameter that sometimes formed flame-shaped tangle-like structures. Immunoelectron microscopy showed that an epitope of alpha B-crystallin was located on the granule-associated filaments composing OCIs. Our studies further support a cooperative role of alpha B-crystallin, ubiquitin and cytoskeletal protein in the formation of some types of intracytoplasmic inclusions.

Adolescent↗

PubMed1992

Increased in vivo production of tumor necrosis factor after development of diabetes in nontreated, long-term diabetic BB rats.

We have recently reported that chronic and systemic administration of tumor necrosis factor alpha (TNF) inhibits development of autoimmune diabetes in NOD mice and BB rats, animal models of insulin-dependent diabetes mellitus (IDDM). During these experiments, we unexpectedly found that in vivo production of TNF stimulated by a single injection of lipopolysaccharide was enhanced approximately 10 times in the long-term diabetic BB rats (P less than 0.0001), whose mean duration of diabetes with more than 16.8 mM (300 mg/dl) of nonfasting blood glucose level was 26.2 +/- 2.1 days, as compared to that in the rats of nondiabetes and in the rats at the onset of diabetes, whose mean duration of diabetes was 1.4 +/- 0.6 days. The long-term diabetic, but not short-term-diabetic, rats were also associated with increased levels of serum fructosamine/albumin (P less than 0.01) and triglyceride (P less than 0.01) and with a decreased level of serum albumin (P less than 0.01). The in vivo TNF productivity in the diabetic rats, including the short-term- and long-term-diabetic rats, was correlated positively with the level of fructosamine/albumin (P less than 0.05) and negatively with the level of serum albumin (P less than 0.05), but not with levels of blood glucose. None of these correlations were observed in nondiabetic rats. The increased LPS-induced serum TNF activity in the long-term diabetic state was observed not only in BB rats but also in NOD mice and GK rats, a model of non-IDDM, irrespective of sexes and ages, indicating that the enhancement of in vivo TNF production was a result of long-term diabetes. These findings indicate that some factor(s) associated with the long-term-diabetic state may prime macrophages in vivo to produce TNF. Further study is needed to reveal a mechanism of the enhanced TNF production and its possible relevance to various abnormalities associated with the chronic hyperglycemic state.

Age Factors↗

PubMed1992

A neuropathological study of a case of the Prader-Willi syndrome with an interstitial deletion of the proximal long arm of chromosome 15.

An autopsy case, a 6-month-old girl, with an interstitial deletion of the long arm of chromosome 15;del(15)(q11.1q12) was reported. Muscle hypotonia, poor sucking and intermittent ocular deviation were noticed soon after birth. She also exhibited external features peculiar to the Prader-Willi syndrome (PWS). The muscle hypotonia persisted and head control was not achieved. She died at the age of 6 months due to bronchopneumonia. G-banding analysis of prometaphase chromosomes revealed a deletion of chromosome 15. Bronchopneumonia of the lungs and fatty metamorphosis of the liver were found. Neuropathological anomalies recognized were; disturbed undulating structures, resembling cortical micropolygyria and pachygyria, in the dentate nucleus and the inferior olivary nucleus, grumose degeneration of the nerve cells in the dentate nucleus, and heterotopia of middle-sized neurons in the cerebellar white matter. No abnormalities were observed in the hypothalamus-pituitary system. In some autopsy cases of PWS, cerebellar lesions have been reported. These might be related to the muscle hypotonia in PWS.

Brain↗

PubMed1992

A neuropathological study of early onset Cockayne syndrome with chromosomal anomaly 47XXX.

We present the clinical and neuropathological findings in a female patient with early onset Cockayne syndrome and a chromosomal anomaly (47XXX). The girl was the only child of healthy, unrelated parents. She was born with a birth weight of 1,930 gm. She had progeroid facial features with bilateral cataracts. A diagnosis of 47XXX was made on the basis of a chromosomal study. Physical shortness became increasingly prominent while her weight remained stationary. Psychomotor retardation was noted, and she could never sit alone. A brain CT scan showed cerebral atrophy and calcification of the basal ganglia. Cultured skin fibroblast exhibited significant sensitivity to the ultraviolet light. She died from a chest infection at the age of 7 years and 4 months. Microscopically, the renal glomeruli showed diffuse sclerotic changes with thick capillary basement membranes. A neuropathological examination revealed a very small brain (295 gm), extensive myelin deficiency, gliosis in the white matter, and calcifications in the basal ganglia, and cerebral and cerebellar cortices. The loss of both Purkinje and granular cells was noticed in the cerebellar cortex. This is the first report of a case with the Cockayne syndrome and 47XXX, and the 47XXX in this patient seems to be coincidental.

Brain↗

PubMed1992

[Prognostic value of urinary cytology in bladder tumor].

Retrospective analysis was carried out to evaluate the prognostic value of urinary cytology in bladder tumor patients. All of the 170 patients (107 superficial (less than T2), 60 advanced (greater than T1) and 3 unknown (TX)), who were followed after their first occurrence, had histologically diagnosed transitional cell tumors. Recurrence rate for superficial cases was higher (p less than 0.05) when urinary cytology, either before or after the initial treatment, was positive than when negative. Patients with positive urinary cytology before the initial treatment proved to show poor prognosis compared to those with negative cytology (p less than 0.01), and many of the positive cases were with advanced cancer. Urinary cytology seemed to be indicative of the neoplastic potential of bladder tumor.

Adult↗