Biomedical subjects

S Kondo

Publications and source records attributed to S Kondo.

At least 541 records · Page 30Linked to original sources

PubMed1995

Cholecystokinin is not a physiological regulator of gastric pepsin secretion in rats.

The physiological relevance of cholecystokinin (CCK) in gastric pepsin secretion is unclear, although CCK has been reported to stimulate pepsin secretion in intact animals and in dispersed chief cell. To clarify the physiological role played by this peptide in pepsin secretion, we determined the effects of intravenous infusions of CCK on gastric pepsin release, and investigated the effect of endogenous CCK released by small amounts of trypsin inhibitor on pepsin secretion in conscious rats. The infusion of CCK-8 at 1 nmol/kg per h resulted in a plasma CCK concentration of 204 pM and a 2.5-fold increase in pepsin secretion compared to the baseline rate. The infusion of CCK-8 at 0.3 nmol/kg per h resulted in a plasma CCK concentration of 41.8 pM and also caused a significant increase in pepsin secretion compared to the baseline rate. However, the infusion of CCK-8 at 0.1 nmol/kg per h (plasma CCK level, 19.9 pM), which is still far beyond the physiological plasma levels of CCK, did not significantly affect pepsin secretion. In addition, the intraduodenal infusion of soybean trypsin inhibitor increased the plasma CCK concentration to 4.4 pM, a value comparable to that observed after feeding (3.3 pM), but again, this had no effect on gastric pepsin secretion. We conclude that CCK is not a physiological regulator of gastric pepsin secretion in rats.

Animals↗

PubMed1995

Luxury perfusion phenomenon in acute herpes simplex virus encephalitis.

In a patient with acute herpes simplex virus (HSV) encephalitis, positron emission tomography (PET) demonstrated increased cerebral blood flow in the affected temporal lobe accompanied by reduction in the cerebral oxygen extraction fraction and the cerebral metabolic rate of oxygen, i.e., luxury perfusion. Follow-up PET studies showed reduction in cerebral perfusion until it was more closely coupled with oxygen metabolism after the resolution of the acute inflammation. These findings support previous single photon emission computed tomographic data and provide a pathophysiological background for the occurrence of hyperperfusion in HSV encephalitis. This is an interesting example of the luxury perfusion phenomenon occurring in a disease other than cerebral ischemia.

Adult↗

PubMed1995

Localization of heparin-binding epidermal growth factor-like growth factor in human gastric mucosa.

BACKGROUND & AIMS: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) has been recently identified as a member of the EGF family. EGF receptors to which HB-EGF can bind have been detected in some types of gastric epithelial cells. The aim of this study was to investigate whether HB-EGF is produced in gastric epithelial cells to maintain normal gastric mucosa. METHODS: Gene expression and production of HB-EGF protein were investigated using Northern hybridization and immunohistochemistry, and the types of cells producing this protein were determined in human gastric mucosa. RESULTS: HB-EGF messenger RNA was detected in the body and antrum. Immunohistochemical staining showed that HB-EGF was localized mainly in parietal cells of fundic glands and in gastrin cells of pyloric glands. Also, the immunoreactivity of EGF receptors was observed in parietal cells and gastrin cells and faintly in surface epithelial cells and mucous neck cells of the proliferative zone. CONCLUSIONS: The results suggest that HB-EGF is synthesized mainly in parietal cells and gastrin cells and may act in an autocrine and/or paracrine manner in the regulation of proliferation and differentiation of the gastric mucosal cells through their surface EGF receptors.

Adult↗

PubMed1995

The role of cis-urocanic acid in UVB-induced suppression of contact hypersensitivity.

Ultraviolet light B (UVB) is well recognized to suppress the contact hypersensitivity (CHS) response and it has been postulated that cis-urocanic acid (UCA) is a mediator of the immunosuppression. This study was designed to examine the effect of UCA on CHS and to clarify its role in UVB-induced immunosuppression in C57BL/6 mice. Intradermal injection of 0.5-50 micrograms cis-UCA into the ear 2 h before DNFB sensitization resulted in a 60-70% reduction of CHS assessed by ear swelling, whereas trans-UCA did not have a significant effect on CHS except at a high dose (50 micrograms) which showed a 20-40% suppression. Intraperitoneal injection of anti-cis-UCA antibody before administration of cis-UCA abrogated the suppression. To examine the effect of UCA on UVB-induced immunosuppression, some mice were pre-treated with anti-cis-UCA antibody and then exposed to UVB (960 J/m2). After 3 days the mice were sensitized either on the irradiated abdominal skin or on the unirradiated dorsal surface of the right ear followed by the challenge on the left ear. The CHS response was significantly suppressed in UVB-irradiated mice both locally (abdominal sensitization, suppression was 45%, P < 0.001) and systemically (ear sensitization, suppression was 53%, P < 0.0025). The CHS response was partially restored in both abdominal sensitized mice and ear sensitized mice by pre-treatment with anti-cis-UCA antibody. These results confirmed the immunosuppressive effects of cis-UCA on CHS and suggest that cis-UCA plays a role in UVB-induced local and systemic immunosuppression.

Animals↗

PubMed1995

Epidermal cytokines in allergic contact dermatitis.

The understanding of cutaneous immunology has grown significantly during the past decade, particularly regarding the immune function of keratinocytes. Keratinocytes play a major role in immune and inflammatory reactions, mainly through synthesis and release of cytokines. The cytokine network in the skin is an important contributor to normal homeostasis and to the pathogenesis of cutaneous disease. Although cytokine dysregulation has been implicated in the pathogenesis of many cutaneous diseases, allergic contact dermatitis is one that has been the most extensively studied. The aim of this article is to provide a comprehensive current review of the mechanisms of allergic contact dermatitis with particular emphasis on the role of epidermal cytokines.

Cytokines↗

PubMed1995

Effects of contact sensitizers neomycin sulfate, benzocaine and 2,4-dinitrobenzene 1-sulfonate, sodium salt on viability, membrane integrity and IL-1 alpha mRNA expression of cultured normal human keratinocytes.

The toxic effect of three potential contact sensitization chemicals [the aminoglycosidic antibiotic neomycin sulfate, the local anaesthetic benzocaine and the primary sensitizer 2,4-dinitrobenzene 1-sulfonate, sodium salt (DNBS)], on cultured human keratinocytes was examined. The three chemicals were compared with respect to their cytotoxic potential (determined by crystal violet staining assay), their membrane disruptive potential ([3H]arachidonic acid release assay), and their effects on interleukin 1 alpha (IL-1 alpha) mRNA expression [reverse transcription-polymerase chain reaction (RT-PCR)]. At the concentrations used, neomycin sulfate (0.004-0.32%) and benzocaine (0.0165-0.165%) did not show relevant cytotoxicity or membrane perturbation. On the other hand, DNBS (0.001-1%) caused a significant dose-dependent cytotoxic response at concentrations higher than 0.1%, while the [3H]arachidonic acid release assay indicated absence of membrane perturbation activity in all the range of DNBS concentrations examined. The effects of the three sensitizers on IL-1 alpha mRNA expression were varied; neomycin sulfate caused a dose-dependent induction of IL-1 alpha mRNA, benzocaine did not significantly affect its signal, and DNBS suppressed IL-1 alpha gene expression.

Arachidonic Acid↗

PubMed1995

Disseminated intravascular coagulation after liver resection: retrospective study in patients with biliary tract carcinoma.

BACKGROUND: Disseminated intravascular coagulation (DIC) after hepatectomy is not well understood. The objective of this retrospective study was to evaluate hemostatic changes after extensive liver resection and to elucidate the frequency of posthepatectomy DIC. METHODS: In 100 patients without cirrhosis who underwent resection of two or more segments of the liver for biliary tract carcinoma, various hemostatic parameters were measured before and after resection, and the liver function of each patient was assessed. RESULTS: In patients with posthepatectomy liver failure, platelet count, fibrinogen concentrations, and prothrombin time were significantly lower than in those without such failure. Serum levels of fibrin degradation product did not differ significantly between the two groups. The minimum platelet count was significantly negatively correlated with serum total bilirubin level. Posthepatectomy DIC occurred in 2.0% of the patients. CONCLUSIONS: After extensive liver resection patients exhibited a decreased platelet count with hepatic dysfunction. However, this condition rarely resulted in DIC, at least in patients without cirrhosis and serious postoperative complications.

Adult↗

PubMed1995

Right or left trisegment portal vein embolization before hepatic trisegmentectomy for hilar bile duct carcinoma.

BACKGROUND: Percutaneous transhepatic embolization of the right portal vein plus the left medial portal branch (R3-PE) and the left portal vein plus the right anterior portal branch (L3-PE) is not well described. METHODS: Four patients with far advanced carcinoma of the hepatic hilus underwent R3-PE (n = 1) or L3-PE (n = 3) as preoperative management for right hepatic trisegmentectomy or left hepatic trisegmentectomy. The portal vein embolization was performed with the ipsilateral approach through the right anterior portal branch. RESULTS: In all patients the embolizations were successful without complications. Volumetric study with computed tomography showed sufficient hypertrophy of the nonembolized hepatic segments. Three of the four patients eventually underwent trisegmentectomy. The postoperative courses in two of the patients were uneventful. The remaining patient suffered from posthepatectomy liver failure but recovered. CONCLUSIONS: R3-PE or L3-PE is advisable as preoperative management for trisegmentectomy and appears effective for increasing the safety of the operation. This embolization is achievable only through the ipsilateral approach.

Adult↗

PubMed1995

Limited TCR V beta usage of infiltrating T cells in synovial tissues from patients with HTLV-I associated arthropathy.

Human T cell lymphotropic virus type-I (HTLV-I) is the etiologic agent of adult T cell leukemia/lymphoma and recently has also been suggested to be involved in chronic arthritis. The synovia of patients with rheumatoid arthritis (RA) contains activated T lymphocytes, with a restricted expression of T cell receptor (TCR) variable (V) beta gene segments. To characterize the T-cell populations of RA among HTLV-I carriers and noncarriers, we performed the immunohistochemical staining of CD4 and CDB, as well as a reverse transcription polymerase chain reaction (RT-PCR) to estimate the proportion of TCR beta RNA containing any particular V elements on the synovial specimens. In all but one HTLV-I carrier, the proviral DNA and/or RNA expression of HTLV-I was detected in the synovium. The CD4-positive cells proliferated markedly in the HTLV-I carriers compared with the noncarriers. In contrast to mononuclear cells in the peripheral blood, synovial T cells expressed only a few V beta transcripts, and no definite difference was observed between the carriers and the noncarriers. These results suggest that a common major antigen associated with the pathogenesis of RA may thus selectively interact with the V beta component of the TCR. Using RT-PCR, we studied the expression of the recombination-activating gene-1 (RAG-1), which was used in the V(D)J recombination of immunoglobulin and TCR genes. In all cases, RAG-1 was transcripted. The results supported the possibility that the extrathymic development of the selected TCR V beta T cells occurred in the synovia.

Adult↗

PubMed1995

Comparative larvicidal activities of the four Bacillus thuringiensis serovars against a chironomid midge, Paratanytarsus grimmii (Diptera: Chironomidae).

The four reference strains of Bacillus thuringiensis, known to be pathogenic for mosquito larvae of the family Culicidae (Diptera), were examined for their larvicidal activities against a chironomid species, Paratanytarsus grimmii (Diptera: Chironomidae). Of the four, the type strain of B. thuringiensis serovar israelensis (H14) exhibited the highest activity against both early- and late-instar larvae, while the type strain of serovar kyushuensis (H11ac) and the strain 73-E-10-2 (H10, serovar darmstadiensis) showed relatively moderate toxicities. The strain HD-1 of serovar kurstaki (H3abc) had no larvicidal activity on this chironomid midge.

Animals↗

PubMed1995

Permeability of peptides and proteins in human cultured alveolar A549 cell monolayer.

PURPOSE: The transport of peptides or proteins across the alveolar cell monolayer was studied in vitro in order to elucidate their transport pathway. METHODS: The permeability of 14 peptides or proteins and 6 dextrans with MW 1,000-150,000 was measured in cultured human lung adenocarcinoma A549 cell monolayers at 37 degrees C or 4 degrees C. The stability of the tested peptides and proteins was also evaluated. RESULTS: The permeability coefficients of these macromolecules across the A549 cell monolayer at 37 degrees C ranged from 10(-5) to 10(-7) (cm/sec), and exhibited a good inverse correlation with molecular weight. All macromolecules were stable throughout the transport experiment, and degradation by proteases was minimal. Permeability at 4 degrees C did not differ from that at 37 degrees C. Clear selectivity for direction of transport was not observed. CONCLUSIONS: These results suggested that the tested peptides and proteins appeared to penetrate the A549 cell monolayer via a paracellular route by passive diffusion.

Adenocarcinoma↗

PubMed1995

Combination therapy with cisplatin and nifedipine induces apoptosis in cisplatin-sensitive and cisplatin-resistant human glioblastoma cells.

We attempted to determine whether calcium channel blockers (CCBs) enhance the anti-tumour activity of cis-diamminedichloroplatinum (cisplatin) against both cisplatin-sensitive human glioblastoma U87 MG cells and cisplatin-resistant U87-MG-CR cells, the latter of which we developed for resistance to cisplatin. Nifedipine, a dihydropyridine class CCB, significantly enhanced the anti-tumour effect of cisplatin on these two cell types in vitro and in vivo. Our findings also indicated that, in the absence of normal extracellular Ca2+ nifedipine was capable of enhancing the cytotoxicity of cisplatin. In addition, this anti-tumour activity was partially inhibited by actinomycin D and cycloheximide, suggesting that it is possibly dependent upon new RNA and protein synthesis. Interestingly, ultrastructural analysis, DNA fragmentation assay and cell cycle analysis demonstrated that synergism between cisplatin and nifedipine results in apoptosis (programmed cell death) at a relatively low concentration of cisplatin, which when tested alone did not induce apoptosis. Furthermore, we demonstrated that nuclei from these cells lack a Ca(2+)-dependent endonuclease that degrade chromatin in the linker region between nucleosomes. In conclusion, our studies suggest that the non-cytotoxic agent nifedipine is able to synergistically enhance the anti-tumour effects of cisplatin on U87-MG and U87-MG-CR cells lacking a Ca(2+)-dependent endonuclease and subsequently to induce apoptosis via interaction of nifedipine with an as yet uncharacterised functional site other than a calcium channel on target cells.

Animals↗

PubMed1995

KIF2 is a new microtubule-based anterograde motor that transports membranous organelles distinct from those carried by kinesin heavy chain or KIF3A/B.

Kinesin is known as a representative cytoskeletal motor protein that is engaged in cell division and axonal transport. In addition to the mutant assay, recent advances using the PCR cloning technique have elucidated the existence of many kinds of kinesin-related proteins in yeast, Drosophila, and mice. We previously cloned five different members of kinesin superfamily proteins (KIFs) in mouse brain (Aizawa, H., Y. Sekine, R. Takemura, Z. Zhang, M. Nangaku, and N. Hirokawa. 1992. J. Cell Biol. 119:1287-1296) and demonstrated that one of them, KIF3A, is an anterograde motor (Kondo, S., R. Sato-Yashitake, Y. Noda, H. Aizawa, T. Nakata, Y. Matsuura, and N. Hirokawa. J. Cell Biol. 1994. 125:1095-1107). We have now characterized another axonal transport motor, KIF2. Different from other KIFs, KIF2 is a central type motor, since its motor domain is located in the center of the molecule. Recombinant KIF2 exists as a dimer with a bigger head and plus-end directionally moves microtubules at a velocity of 0.47 +/- 0.11 microns/s, which is two thirds that of kinesin's. Immunocytological examination showed that native KIF2 is abundant in developing axons and that it accumulates in the proximal region of the ligated nerves after a 20-h ligation. Soluble KIF2 exists without a light chain, and KIF2's associated-vesicles, immunoprecipitated by anti-KIF2 antibody, are different from those carried by existing motors such as kinesin and KIF3A. They are also distinct from synaptic vesicles, although KIF2 is accumulated in so-called synaptic vesicle fractions and embryonal growth cone particles. Our results strongly suggest that KIF2 functions as a new anterograde motor, being specialized for a particular group of membranous organelles involved in fast axonal transport.

Animals↗

PubMed1995

Isolation and characterization of neutralizing monoclonal antibodies to human vascular endothelial growth factor/vascular permeability factor121 (VEGF/VPF121).

We have established monoclonal antibodies (MAbs) against human vascular endothelial growth factor/vascular permeability factor121 (VEGF/VPF121). Two (MV101 and MV303) of the 28 MAbs neutralized the mitogenic activity of VEGF/VPF121 on human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. Both of the MAbs reacted to VEGF/VPF121 and also VEGF/VPF165 with somewhat different binding properties in a sandwich-type enzyme-linked immunosorbent assay (ELSIA). The binding of MV101 and MV303 to VEGF/VPF121 was competitive, but MV415, another anti-VEGF/VPF121 MAb without neutralizing activity, did not complete with either of the antibodies. MV101 and MV303 specifically recognized the native form of VEGF/VPF121 and VEGF/VPF165 in Western blotting. They did not react with VEGF/VPF when the antigens were fractionated under reducing conditions. These observations suggested that MV101 and MV303 might recognize the epitopes closely located on the configuration of VEGF/VPF121 molecule and the epitopes recognized by MV101 and MV303 may play an important role in the VEGF/VPF-receptor signal transduction. These MAbs significantly suppressed the growth of a human hepatoma, PLC/PRF/5, in vivo.

Animals↗

PubMed1995

Different localization of tau protein kinase I/glycogen synthase kinase-3 beta from glycogen synthase kinase-3 alpha in cerebellum mitochondria.

We examined the subcellular distribution of two glycogen synthase kinase-3 (GSK-3) isoforms in rat cerebellum. Results from immunoelectron microscopy and subcellular fractionation revealed that one isoform, tau protein kinase I/GSK-3 beta (TPKI/GSK-3 beta), was present in mitochondria, but GSK-3 alpha was not. Although the two GSK-3 isoforms seem to have similar properties, the difference of subcellular localization observed here suggests that TPKI/GSK-3 beta fulfills some specific function in mitochondria.

Animals↗

PubMed1995

Expression of SQ10 (a preprorelaxin-like gene) in the pregnant rabbit placenta and uterus.

A Northern blot containing poly(A)+ RNA isolated from pregnant rabbit placenta, uterus, ovary, mammary gland, psoas muscle, and intestine was hybridized with an oligonucleotide probe to porcine preprorelaxin. Only the placenta and uterus exhibited high levels of a 1-kb mRNA that hybridized to the probe. Porcine preprorelaxin primers were used to generate and amplify cDNAs from placental and uterine poly(A)+ RNA. Southern blot analysis of the placental and uterine cDNAs each revealed a single PCR product that hybridized with the porcine relaxin probe. The sequence of the cDNAs exhibited 100% identity with SQ10, a preprorelaxin-like gene identified in rabbit tracheobronchial epithelial cells. Identical results were obtained with primers specific for SQ10. SQ10 is expressed in tracheobronchial epithelial cells during abnormal conditions, such as mechanical or toxic injury. The protein is believed to have a role in tracheal epithelial cell differentiation and transformation that occurs under the above conditions. This work shows, for the first time, the presence of high levels of message for SQ10 in normal reproductive tissues. The expression of SQ10 in the uterus and placenta may suggest an important role in cell differentiation and transformation that occurs in these tissues during pregnancy.

Amino Acid Sequence↗

PubMed1995

An immunohistochemical study of lysozyme, CD-15 (Leu M1), and gross cystic disease fluid protein-15 in various skin tumors. Assessment of the specificity and sensitivity of markers of apocrine differentiation.

We investigated immunohistochemically the localization of lysozyme and Leu M1 in normal skin, 76 cases of benign sweat gland tumors, 28 cases of malignant sweat gland tumors, 23 cases of extramammary Paget's disease, 7 cases of sebaceous carcinoma, 6 cases of malignant trichilemmoma, 10 cases of squamous cell carcinoma, and 10 cases of basal cell carcinoma and compared the results with those for gross cystic disease fluid protein (GCDFP)-15 to assess the sensitivity and specificity of our assay conditions for apocrine differentiation. Normal apocrine glands were stained with all three antibodies, while eccrine glands were positive only for GCDFP-15, and other portions of normal skin were not stained with any of the antibodies used. In neoplastic tissue thought to be from apocrine tumors, antibodies raised against lysozyme and GCDFP-15 had a greater specificity (100%) for apocrine differentiation, while Leu M1 had a greater sensitivity (88%). Tissues that were stained with two or three of these antibodies appeared to exhibit apocrine differentiation. In the tumors examined, the specificity for apocrine differentiation was 100% and the sensitivity for such differentiation was 92% by these criteria. According to these criteria, some cases of syringocystadenoma papilliferum, primary mucinous carcinoma of the skin, and extramammary Paget's disease with underlying adenocarcinoma showed apocrine differentiation.

Adenocarcinoma↗

PubMed1995

Typing of Staphylococcus aureus colonising human nasal carriers by pulsed-field gel electrophoresis.

Colonisation by Staphylococcus aureus in the nares of 120 outpatients and 63 healthy adults was studied for c. 2 years. Two states of carriage of S. aureus were confirmed: persistent carriage and persistent non-carriage. The states of carriage and non-carriage were quite stable and > 60% of the population of any of the study groups were stable non-carriers. The results of typing the strains isolated from the same individuals at different times with DNA fingerprinting by digestion with SmaI enzyme showed that all the stable carriers were persistently infected with the same strain and that changes in the strain seldom occurred.

Adult↗