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Biomedical subjects

K Hirata

Publications and source records attributed to K Hirata.

At least 325 records · Page 18Linked to original sources
PubMed1999

[Cerebral infarction accompanied by dysgeusia--a clinical study on the gustatory pathway in the CNS].

Dysgeusia was investigated in 11 patients with thalamic infarction and 13 patients with corona radiata infarction to locate the gustatory pathways based on the sites of the lesions. Dysgeusia was present in 4 out of 11 patients with thalamic infarction and 3 out of 13 patients with corona radiata infarction. The dysgeusia was contralateral to the lesion in all these patients. Cheiro-oral syndrome was observed as a complication in 2 patients each from both groups. The responsible lesion was located on the medial side of the ventral posterolateral (VPL) nucleus and the ventral posteromedial (VPM) nucleus in the patients with thalamic infarction who developed dysgeusia, and was located posteriorly to the corona radiata in the other group. In the patients without gustatory disturbance, on the other hand, the lesions showed no such spread. These findings suggest that the gustatory pathway ascends contralaterally in the cerebral hemisphere and that the pathway from the thalamus projects to the cerebral cortex via the posterior part of the corona radiata. It is also suggested that the pathways in the thalamus and corona radiata are very close to the sensory fibers from the mouth and hands projecting to the sensory area.

Aged↗
PubMed1999

[Combination chemotherapy of continuous infusion 5-FU and daily low-dose CDDP in colorectal carcinoma].

Continuous intravenous infusion (CVI) of 5-fluorouracil (5-FU) plus daily low-dose cisplatin (CDDP) was evaluated in 59 patients with advanced and unresectable colorectal carcinoma. The procedure consisted of 5-FU 320 mg/m2/day, CVI and CDDP 2.5-3.5 mg/m2/day, infused for one hour five times a week (low-dose FP therapy) was performed for at least four weeks. The rates of complete and partial response, along with side effects were studied. Also, the effect of low-dose FP therapy on the prognosis of patients with colorectal carcinoma was investigated. The rate of complete and partial response was 57.1%. The frequency of severe side effects (grade 3 and 4) was 10.5%, and no death from side effects was noted. The effect of low-dose FP therapy on the prognosis of advanced and unresectable colorectal carcinoma was studied. It is suggested that this chemotherapy might contribute to the survival of patients with colorectal carcinoma. We designed the chemotherapy of intermittent administration (day by day) of 5-FU 600 mg/m2/day and daily CDDP 2.5-3.5 mg/m2/day (intermittent FP) in order to decrease the rate of side effects and their severity. No cases with grade 3 or 4 side effects were experienced, but the response rate was mostly similar to that of low-dose FP therapy. We concluded that low-dose FP and intermittent FP therapy might be fairly effective for advanced and unresectable colorectal carcinoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

[Mechanisms of cell death in hypoxic stress].

The present article attempts to summarize and introduce the mechanisms of hypoxia-induced cell death. Necrosis is associated with rapid metabolic collapse that leads to cell swelling, early loss of plasma membrane integrity, and ultimate cell rupture, in which cytosolic contents leak from necrotic cells causing injury to and inflammation of the surrounding tissue. In contrast, apoptosis is an energy-requiring, gene-directed process, which results in cell suicide without any injury to surrounding tissues. Although apoptosis and necrosis are conceptually distinct pathways of cell death, recent advances have revealed that hypoxic cell damage can induce both necrosis and apoptosis simultaneously. Loss of the mitochondrial membrane potential (MMP) precedes the morphological changes in cell death, and overexpression of Bcl-2 or Bcl-XL blocks apoptosis as well as hypoxia-induced necrosis by maintaining MMP. These findings indicate that apoptosis and some types of necrosis share common features in the death signaling pathway. The factors that determine whether cells undergo apoptosis or necrosis are still unclear, but intracellular ATP levels and/or their rate of decline are considered to be one possible determinant of the manifestation of cell death.

Adenosine Triphosphate↗
PubMed1999

[A case report of valproate encephalopathy].

A 24-years-old woman with epilepsy treated with valproic acid developed disorientation, acalculia, perseveration, slow responsiveness and loss of memory. The drug withdrawal induced a quick improvement of mental function. In this case, hyperammonemia, hypocarnitinemia, increased protein in cerebrospinal fluid were found. When the drug was discontinued, she had a dramatic improvement. Valproic acid caused encephalopathy because of metabolic abnormality in mitochondria in this case. In the cases of encephalopathy caused by valproic acid, the drug administration should be withdrawn, and appropriate measures had to be taken. In addition, elevation of ammonia in the blood, lactic acid and pyruic acid in the serum and cerebrospinal fluid, and decreased carnitine level in the serum will be useful to make a diagnosis of valproate-induced encephalopathy.

Adult↗
PubMed1999

A prostaglandin E1 analog, OP-1206, alleviates 5-fluorouracil-induced injury of rat small intestine.

5-Fluorouracil (5-FU) often causes the gastrointestinal toxicity, including enterocolitis. We investigated effects of OP-1206 (17S, 20-dimethyl-trans-delta2-prostaglandin E1) on 5-FU-induced leukocyte infiltration and epithelial barrier dysfunction of rat small intestine. Myeloperoxidase (MPO) activity of the small intestine was assayed as an index of leukocyte infiltration. Intestinal epithelial permeability was determined by the small intestinal absorption of a paracellular permeation marker, fluorescein isothiocyanate-labeled dextran (molecular weight; 4,400) (FD-4) using the in situ closed intestinal loop technique. The MPO activity and FD-4 permeation were significantly increased by the administration of 5-FU to rats for 4 days, while on the coadministration of 5-FU and OP-1206, they were similar to those of control rats treated with saline solution alone, respectively. These observations indicate that OP-1206 reduced the leukocyte infiltration and the change in epithelial permeability of rat small intestine induced by 5-FU.

Alprostadil↗
PubMed1998

Fisher's syndrome and group A streptococcal infection.

Group A beta-hemolytic streptococcus causes immune-mediated disorders such as acute rheumatic fever and acute glomerulonephritis. We describe a second patient with Fisher's syndrome (FS) from whom beta-hemolytic streptococcus was isolated. We performed a study of the antecedent pharyngeal symptoms in FS and Guillain-Barré syndrome. Sore throat was statistically more frequent in FS (18/24 cases, 75%) than in Guillain-Barré syndrome (29/58 cases, 50%). In a series, however, the association of FS with group A streptococcal infection was not shown. Some patients may develop FS after group A streptococcal infection, but the bacterium is not a major antecedent agent in FS.

Adolescent↗
PubMed1998

Guillain-Barré and Fisher's syndromes subsequent to Campylobacter jejuni enteritis are associated with HLA-B54 and Cw1 independent of anti-ganglioside antibodies.

The frequencies of human leukocyte antigens (HLA)-class I (A, B and Cw) were determined serologically and those of HLA-class II (DRB1 and DQB1) at the genomic level in 35 Japanese patients with Guillain-Barré syndrome (GBS), 58 with Fisher's syndrome (FS), and 112 healthy controls. HLA-B54 and -Cw1 antigens were found in GBS and FS patients from whom Campylobacter jejuni had been isolated more often than found in the healthy controls. No HLA types were related to GBS or FS as a whole, except for the B54 antigen which often was significant in the entire GBS group. This relation, however, may depend on the high population of C. jejuni-isolate patients in our GBS group. There were no relationships between the frequencies of HLA types and the presence of serum IgG antibodies to GM1, GQ1b, GD1a, or GalNAc-GD1a. Our findings suggest that HLA types are associated with the onset of GBS and FS after C. jejuni enteritis and that the HLA types in distinct GBS and FS subgroups of a single etiological origin need to be examined.

Antibodies↗
PubMed1998

Enhancement of metastatic activity of colon cancer as influenced by expression of cell surface antigens.

BACKGROUND: Cell surface antigens are contributory factors toward metastatic activity. There have been no detailed studies on changes in cell surface antigens of colon cancer cell lines. To control life-threatening metastasis, it is necessary to evaluate what types of changes in cell surface antigens exert an influence on metastatic activity. MATERIALS AND METHODS: In vivo selection was performed using the human colon cancer-derived cell line KM12SM to obtain variants of metastatic activity. A murine spleen injection-liver metastasis procedure reflecting the latter half of the metastatic process was adopted and repeated four times. Flow cytometric analyses were carried out to detect expression of antigens: Lewis a (Lea), Lewis x (Lex), sialyl Lewis a (sLea), sialyl Lewis x (sLex), E-cadherin, CD44v6, integrin alpha2 (CD49b), integrin alpha3 (CD49c), integrin alpha4 (CD49d), integrin alpha5 (CD49e), and integrin beta1 (CD29). RESULTS: In vivo selection produced variants with higher metastatic activity. In the original line KM12SM, sLea, E-cadherin, CD49b, CD49c, or CD29 were positive in more than 40% of the cells. After selection, the percentage of cells positive for Lea, sLea, and all examined integrins significantly increased. Lex, sLex, and CD44v6 increased slightly, while E-cadherin decreased slightly. CONCLUSIONS: In vivo selection and flow cytometric analysis revealed that Lea, sLea, CD49b, CD49c, and CD29 appear to be involved in the increase of metastatic activity. The changes of integrin expression in this study suggest that integrins collaborate in the promotion of adhesion to an extracellular matrix.

Animals↗
PubMed1998

Novel paracrine signaling mechanism in the ocular ciliary epithelium.

The ciliary body contains an epithelial bilayer consisting of an outer pigmented cell layer (PE) and an inner nonpigmented cell layer (NPE) responsible for aqueous humor secretion. Secretion may be mediated in part by cytosolic Ca2+ concentration ([Ca2+]i), but whether or how the two layers could coordinate their Ca2+ signals to regulate secretion is unclear. To investigate interactions between PE and NPE, we examined [Ca2+]i signaling in isolated intact ciliary epithelial bilayers using confocal microscopy. Phenylephrine selectively increased [Ca2+]i in PE and acetylcholine increased [Ca2+]i in NPE, but epinephrine increased [Ca2+]i in both layers. This increase spread from PE to NPE, and [Ca2+]i signaling across the bilayer remained coordinated during [Ca2+]i oscillations. All epinephrine-induced [Ca2+]i signaling was blocked by the alpha1-adrenergic antagonist prazosin, whereas signaling in the NPE but not PE was blocked by the beta-adrenergic antagonist propranolol, the gap junction blockers octanol and 18alpha-glycyrrhetinic acid, or the A kinase inhibitor Rp diastereomer of adenosine 3',5'-cyclic monophosphothioate. The beta-adrenergic agonist isoproterenol failed to increase Ca2+ by itself, but isoproterenol plus phenylephrine-induced [Ca2+]i signals across the bilayer similar to those induced by epinephrine. Finally, isoproterenol increased cell-to-cell spread of lucifer yellow via gap junctions, whereas cell-to-cell spread of [Ca2+]i signals could be induced by photorelease of caged inositol 1,4,5-trisphosphate. Thus, calcium signals are coordinated in the epithelial bilayer so that adrenergic stimulation can increase [Ca2+]i in NPE, but only if NPE are primed by activation of endogenous adenylyl cyclase, whereupon they receive stimulation from adjacent PE via gap junctions. This novel interplay between endocrine and paracrine pathways may coordinate [Ca2+]i signaling across the ciliary epithelial bilayer.

Animals↗
PubMed1998

Is IgG anti-GT1a antibody associated with pharyngeal-cervical-brachial weakness or oropharyngeal palsy in Guillain-Barré syndrome?

The pharyngeal-cervical-brachial variant (PCB) of Guillain-Barré syndrome (GBS) has clinical features similar to those of botulism and diphtheria. Mizoguchi et al. (1994) [Mizoguchi, K., Hase, A., Obi, T., Matsuoka, H., Takatsu, M., Nishimura, Y., Irie, F., Seyama, Y., Hirabayashi, Y., 1994. Two species of antiganglioside antibodies in a patient with a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. J. Neurol. Neurosurg. Psychiatry 57, 1121-1123] reported a patient with PCB-like symptoms who had serum IgG anti-GT1a antibodies which did not cross-react with GQ1b. We assumed that PCB is associated with anti-GT1a antibodies that do not have reactivity to GQ1b and made a serological study of a PCB patient. We searched for PCB patients prospectively and found one with PCB. This patient had IgG anti-GT1a antibodies which were not absorbed with GQ1b in an absorption study, whereas IgG anti-GT1a antibodies from Fisher's syndrome patients were. The frequency of positive IgG anti-GT1a antibody did not differ in patients with and without bulbar palsy. Our findings indicate that IgG anti-GT1a antibodies which do not cross-react with GQ1b are specifically detectable in PCB and can be used as a diagnostic marker of PCB.

Adult↗
PubMed1998

Expression of NOS, PSA-N-CAM and S100 protein in the granule cell migration pathway of the adult guinea pig forebrain.

To investigate the possible role of nitric oxide (NO) in adult neurogenesis and neuron-glial migration in the rostral migratory stream (RMS), we used a double-labeled immunofluorescence technique together with confocal laser scanning microscopy, and examined the localization of nitric oxide synthase (NOS), the highly polysialylated isoform of neural cell adhesion molecule (PSA-N-CAM), and the astroglial marker in brain, S100 protein (S100), throughout the length of the subependymal layer (SEL) to olfactory bulb (OB) pathway of the adult guinea pig forebrain. Blast-like, beaded, clustered immature cellular elements stained for PSA-N-CAM and those having a typical astrocytic phenotypes positive for S100 protein were densely interlaced throughout the entire length of the SEL. Some S100 positive ependymoglial cells (tanycytes) gave off their basal projections into the closely packed PSA-N-CAM immunopositive clusters in the rostral extension of the subependymal zone (SEZre). The SEL was devoid of NOS immunoreactivity. A dense network of punctate, fenestrated and radially oriented immature cellular elements positive both for NOS and PSA-N-CAM intermingled and overlapped in the inner part of the internal granular layer (IGr), whereas in the outer part, PSA-N-CAM expression gradually diminished and the cells shifted to mature bipolar, spherical or spindle-shaped granule cells with uniform cellular contours, which were exclusively immunopositive for NOS. Radially oriented astroglial phenotypes were intertwined with PSA-N-CAM neuronal clusters in the SEL, and were closely apposed to NOS neuronal elements in the IGr. In summary, these results showed a distinct separation of neurons and glia as revealed by PSA-N-CAM and S100 protein immunostaining, and an inverse spatio-temporal correlation of expression between PSA-N-CAM (immature neuroblasts) and NOS (mature neurons) in the adult guinea pig RMS.

Animals↗
PubMed1998

Ability to remove immunoglobulins and anti-ganglioside antibodies by plasma exchange, double-filtration plasmapheresis and immunoadsorption.

In Japan, patients with Guillain-Barré (GBS) and Fisher's (FS) syndromes often receive plasma exchange (PE), double-filtration plasmapheresis (DFPP), or immunoadsorption (IA). To determine whether DFPP and IA are as effective as PE, we compared their abilities to remove immunoglobulins and anti-ganglioside antibodies. Plasma samples were obtained from 55 GBS patients and 53 FS patients, before and after each session of the treatments. PE decreased the IgG concentration more than DFPP did, its abilities to remove anti-ganglioside IgG antibodies in PE markedly being superior to the abilities of the other plasmaphereses. IA on a tryptophan-immobilized column adsorbed anti-ganglioside IgG antibodies more effectively than IA on other affinity columns.

Adult↗
PubMed1998

Separate determination of human urinary conjugated and unconjugated 3-methoxy-4-hydroxyphenylethyleneglycol.

A new determination procedure for human urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) was established. In addition to the previously established solid-phase extraction method for unconjugated MHPG, another solid-phase extraction method for conjugated MHPG was developed. Unconjugated MHPG was adsorbed on a Sep-Pak Diol cartridge and selectively recovered by elution with ethyl acetate. The eluate was evaporated and the residue was redissolved and analyzed by reversed-phase high-performance liquid chromatography with fluorimetric detection. Conjugated (sulfate plus glucuronide) MHPG was adsorbed on a Sep-Pak Accell QMA cartridge and quantitatively eluted with 0.2 M NaCl. After enzymatic hydrolysis, deconjugated MHPG was extracted using a Sep-Pak Diol cartridge and analyzed in the same manner as unconjugated MHPG. The new method is simple and rapid and can quantitate conjugated and unconjugated MHPG discriminatively.

Adult↗
PubMed1998

Interleukin-10 reduces natural killer sensitivity and downregulates MHC class I expression on H-ras-transformed cells.

We examined the effect of IL-10 on sensitivity to NK-cell-mediated cytotoxicity of the H-ras-induced transformants, W14 and W31. Incubation of cells with recombinant human (rh) IL-10 resulted in a dose-dependent decrease in the expression of MHC class I antigens, but not in the ICAM-1 expression. However, prior incubation of W31 cells with rhIL-10 markedly decreased their susceptibility to cytolysis by rat splenic NK cells. This fact suggested that the IL-10-mediated decrease in MHC class I expression might not dominate the regulation of the NK sensitivity. This was true when rat IL-10 cDNA-introduced W31 cells were used as an endogenous IL-10 producer. The NK sensitivity in vitro of W31T-H, a high IL-10-producer clone, was suppressed downward to the equivalent level of W31 cells pretreated with exogenous rhIL-10. The decreased NK-sensitivity of W31T-H cells was further confirmed by in vivo Winn assay, in which nude mice challenged with W31T-H cells and rat NK cells together developed tumors, whereas nude mice challenged with W31T-L, a minimal-IL-10 producer clone, and NK cells did not. Since neither exogenous nor endogenous IL-10 affected the proliferation of W31 cells, the data indicated that W31T-H cells could evade the NK-cell-mediated immune response in vivo. Taken together, our data reveal a novel mechanism for an IL-10-mediated escape of tumor cells from host immune system by NK cells.

Animals↗
PubMed1998

Carcinoma arising from ectopic pancreas in the stomach: endosonographic detection of malignant change.

We present a case of a submucosal tumor in the stomach that was suspicious for malignancy on preoperative endosonography. The resected tumor was histologically diagnosed as a ductal adenocarcinoma that originated in ectopic pancreatic tissue in the gastric wall. Although malignant transformation in ectopic pancreas is extremely rare, it remains an important consideration in the differential diagnosis of gastric submucosal masses.

Adenocarcinoma↗
PubMed1998

Effects of a low-protein diet on prolactin- and growth hormone-producing cells in the rat pituitary gland.

BACKGROUND: It is well known that an unbalanced diet induces various changes in the pituitary gland. However, little attention has been paid to the molecular aspects of this perturbation. We studied the influence of a low-protein diet (LPD) on the prolactin (PRL) and growth hormone (GH) cells in the rat pituitary gland using immunohistochemical staining and in situ hybridization. MATERIALS: Rats aged 20 days were fed a diet containing 27% protein or one with 8% protein (LPD) for 30 days. Pituitary glands were obtained and subjected to either immunohistochemistry or in situ hybridization. Quantitative morphological analysis was then conducted to determine cell number and area as well as the percentage of cells stained by the respective antisera and/or cDNA probe in each experimental group. RESULTS: The average sectional areas of both PRL- and GH-producing cells in the LPD group were smaller in size than those in the controls. The cell numbers per unit area (mm2) of PRL-positive cells and PRL mRNA-positive cells were 3,596.5 and 3,948.6, respectively, in the LPD group, and 3,179.6 and 4,888.5, respectively, in the controls. The numbers per unit area of GH-positive cells and GH mRNA-positive cells in the LPD group were similar (2,252.3 and 2,224.4), as compared to 2,161.3 and 1,684.2, respectively, in the well-fed rats. Whereas PRL-positive cells comprised about 27% of the total number of cells in both animal groups, those given the LPD contained a lower percentage (29%) of PRL mRNA-positive cells as compared to the controls (44%). On the other hand, GH mRNA-positive cells numbered about 15% of the total cell population both animal groups; however, the malnourished rats contained a lower percentage (16%) of GH-positive cells than did their well-fed counterparts (20%). CONCLUSIONS: Taken together, these results indicate that in the rat pituitary gland, administration of an LPD reduced the size of PRL- and GH-positive cells as well as differentially affecting a subpopulation of the PRL mRNA-positive cells and the GH-positive cells.

Animals↗