[High resolution CT findings in two adults with varicella pneumonia].
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Adult↗
Biomedical subjects
H Ueda
Publications and source records attributed to H Ueda.
Frequent association of 22q11.2 deletion with tetralogy of Fallot.
Chromosome 22q11.2 deletion causes DiGeorge syndrome, velocardiofacial syndrome, conotruncal anomaly face syndrome with tetralogy of Fallot (TOF), and sporadic or familial TOF. To determine the prevalence and clinical importance of the 22q11.2 deletion in TOF, a series of 212 Japanese TOF patients was studied. The type of pulmonary blood supply, which may lead to various clinical outcomes, and other additional anomalies were evaluated clinically. The 22q11.2 deletion was diagnosed by fluorescence in situ hybridization with N25 and TUPLE1 probes. Of the 212 patients examined, 28 (13%) had a 22q11.2 deletion, the frequency being higher than that in TOF patients with trisomy 21. The prevalence of the deletion in TOF patients with pulmonary atresia (PA) plus major aortico-pulmonary collateral arteries (MAPCA) was significantly higher than the value in patients with PA plus patent ductus arteriosus (PDA) (P = 0.04) or with pulmonary stenosis (PS) (P < 0.0001). All 28 patients with 22q11.2 deletion had one or more extracardiac abnormalities. Four of 9 patients with the 22q11.2 deletion and TOF-PA-MAPCA suffered from bronchomalacia, while none of 19 patients with TOF-PA-PDA or TOF-PS manifested bronchomalacia (P = 0.006). These results indicate that 22q11.2 deletion is the most frequent cause of syndromic TOF, especially for TOF-PA-MAPCA, and bronchomalacia is the clinically most important associated anomaly in TOF-PA-MAPCA patients.
Adolescent↗
Hypersensitivity of cerebral artery response to catecholamine in patients with neurally mediated syncope induced by isoproterenol.
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Adolescent↗
Serum-free induced neuronal apoptosis-like cell death is independent of caspase activity.
Cultured cortical neurons survived in a density-dependent manner under serum-free conditions. Low-density cultured cells died in an aurintricarboxylic acid (ATA)-sensitive manner, which was accompanied with marked chromatin condensation and nuclear fragmentation. These features, characteristic for apoptosis, were not attenuated by DEVD-CHO, a caspase-3-specific inhibitor, or zVAD-FMK, a broad range caspase inhibitor, while zVAD-FMK showed a marked inhibition of camptothecin-induced cell death. Therefore, cortical neurons died in an apoptosis-like and a caspase-independent manner under serum-free conditions.
Amino Acid Chloromethyl Ketones↗
G(i1) and G(oA) differentially determine kinetic efficacies of agonists for kappa-opioid receptor.
We examined the diversity of single receptor function by measuring receptor-G protein coupling in the baculovirus-Sf21 expression system. In comparative studies using Sf21 cell membranes expressing kappa-opioid receptor (KOR) plus Galpha(i1)beta(1)gamma(2) or KOR plus Galpha(oA)beta(1)gamma(2), there was no significant difference between both preparations in the K(i) values of various kappa-opioid ligands for the displacement of [(3)H]U69593 binding. However, a marked difference in the rank order of agonists to stimulate [(35)S]GTPgammaS binding was observed between both preparations. These findings suggest that agonist efficacy is dependent on the population of different G proteins expressed in various tissues.
Animals↗
Inhibitory effects of sesquiterpenes from bay leaf on nitric oxide production in lipopolysaccharide-activated macrophages: structure requirement and role of heat shock protein induction.
The methanolic extract from the leaves of Laurus nobilis (bay leaf, laurel) was found to inhibit nitric oxide (NO) production in lipopolysaccharide (LPS)-activated mouse peritoneal macrophages. Through bioassay-guided separation, fourteen known sesquiterpenes were isolated from the active fraction and were examined for ability to inhibit the NO production. Seven sesquiterpene lactones (costunolide, dehydrocostus lactone, eremanthine, zaluzanin C, magnolialide, santamarine and spirafolide) potently inhibited LPS-induced NO production (IC50 = 1.2 approximately 3.8 microM). Other sesquiterpene constituents also showed the inhibitory activity (IC50 > or = 21 microM), but their inhibitory activities were less than those of sesquiterpene lactones. Alpha-methylene-gamma-butyrolactone also showed inhibitory activity (IC50 = 9.6 microM), while mokko lactone and watsonol A etc., reductants of the alpha-methylene-gamma-butyrolactone moiety by NaBH4 or DIBAL, and a 2-mercaptoethanol adduct of dehydrocostus lactone showed little activity (IC50 > or = 18 microM). These results indicated that the alpha-methylene-gamma-butyrolactone moiety is important for the activity. Furthermore, costunolide and dehydrocostus lactone inhibited inducible nitric oxide synthase (iNOS) induction in accordance with induction of heat shock protein 72 (HSP 72). These results suggested that, as one of their mechanisms of action, sesquiterpene lactones induce HSP 72 thereby preventing nuclear factor-kappaB activation followed by iNOS induction.
Animals↗
Suppression of Pyk2 kinase and cellular activities by FIP200.
Proline-rich tyrosine kinase 2 (Pyk2) is a cytoplasmic tyrosine kinase implicated to play a role in several intracellular signaling pathways. We report the identification of a novel Pyk2-interacting protein designated FIP200 (FAK family kinase-interacting protein of 200 kD) by using a yeast two-hybrid screen. In vitro binding assays and coimmunoprecipitation confirmed association of FIP200 with Pyk2, and similar assays also showed FIP200 binding to FAK. However, immunofluorescent staining indicated that FIP200 was predominantly localized in the cytoplasm. FIP200 bound to the kinase domain of Pyk2 and inhibited its kinase activity in in vitro kinase assays. FIP200 also inhibited the kinase activity of the Pyk2 isolated from SYF cells (deficient in Src, Yes, and Fyn expression) and the Pyk2 mutant lacking binding site for Src, suggesting that it regulated Pyk2 kinase directly rather than affecting the associated Src family kinases. Consistent with its inhibitory effect in vitro, FIP200 inhibited activation of Pyk2 and Pyk2-induced apoptosis in intact cells, which correlated with its binding to Pyk2. Finally, activation of Pyk2 by several biological stimuli correlated with the dissociation of endogenous FIP200-Pyk2 complex, which provided further support for inhibition of Pyk2 by FIP200 in intact cells. Together, these results suggest that FIP200 functions as an inhibitor of Pyk2 via binding to its kinase domain.
3T3 Cells↗
Immunolocalization of dystrobrevin in the astrocytic endfeet and endothelial cells in the rat cerebellum.
Dystrobrevin is a newly discovered dystrophin-associated protein that is classified as alpha- and beta-dystrobrevin. Previous studies reported that dystrophin, utrophin, syntrophin and beta-dystroglycan were expressed in the cerebellum. In the present study, we examined cellular and subcellular localization of dystrobrevin in the adult rat cerebellum immunohistochemically. Confocal microscopy showed that dystrobrevin was expressed around blood vessels and under the pia mater as dystrophin, utrophin and beta-dystroglycan were. Immunoelectron microscopy demonstrated that dystrobrevin was localized not only in the astrocytic endfeet around blood vessels and under the pia mater, but also in endothelial cells. Considering the fact that dystrobrevin possesses multiple phosphotyrosine kinase residues, these data suggest that dystrobrevin plays a role in blood-brain barrier functions as a component of the dystrophin complex.
Animals↗
Meeting future challenges in topical ocular drug delivery: development of an air-interfaced primary culture of rabbit conjunctival epithelial cells on a permeable support for drug transport studies.
The purpose of this study was to develop and characterize a functional air-interfaced primary culture of rabbit conjunctival epithelial cells grown on a permeable support for drug transport studies. Conjunctival epithelial cells from the pigmented rabbit were isolated, seeded at 1.2 x 10(6) cells cm(-2) on permeable Transwell filters, and cultured at the air interface using a modified PC-1 medium. Conjunctival epithelial cell layers showed a transepithelial resistance of 1.1+/-0.1 kOmega cm(2), a potential difference of 17.0+/-0.5 mV, and an equivalent short-circuit current (I(eq)) of 16.1+/-0.4 microA cm(-2). The I(eq) was reduced by 35% using 0.01 mM bumetanide, 66% using 0.1 mM ouabain, 46% using 2 mM barium chloride (all three in the basolateral fluid), and 63% using 0.3 mM NPAA in the apical fluid, consistent with active Cl(-)-secretion across the conjunctival epithelial barrier. Amiloride-sensitive Na(+) channels were absent. The permeability of the cell layers to polar solutes decreased with increased solute size, and the calculated equivalent pore size was about 8.0 nm. The Papp of beta-blockers varied with lipophilicity in a sigmoidal fashion. Uridine transport showed temperature sensitivity and directionality, favoring transport in the apical-to-basolateral direction. Apical L-carnosine uptake was reduced by 46% in the absence of an inwardly directed proton gradient, and lowering the temperature to 4 degrees C abolished direction-dependent L-carnosine uptake. Furthermore, uptake was inhibited by 73% using apical 10 mM glycyl sarcosine (a dipeptide transporter substrate) and by 60% using 1 mM L-valacyclovir (a dipeptide prodrug). In conclusion, a functional air-interfaced primary culture of rabbit conjunctival epithelial cell layers was established. This air-interfaced primary culture model may be useful for studying passive and active transport processes for ion and solute translocation in the mammalian conjunctival epithelial barrier in a defined experimental setting.
Adrenergic beta-Antagonists↗
Vzg-1/lysophosphatidic acid-receptor involved in peripheral pain transmission.
The nociception by intraplantar (i.pl.) lysophosphatidic acid (LPA) injection was significantly, but partially blocked when mice received intrathecal (i.t.) antisense oligodeoxynucleotide treatment for the vzg-1 type LPA-receptor. The residual LPA-nociception observed under the condition of pertussis toxin-treatment, which is expected to block presynaptic contribution, was abolished by diphenhydramine (i.pl.), an H1-type histamine receptor antagonist. Taking into account that vzg-1 mRNA was detected in the dorsal root ganglion by RT-PCR method, these findings suggest that the LPA-induced nociception is attributed to the mechanism through vzg-1 receptor on nociceptor endings, and to that through unidentified LPA-receptor on peripheral, possibly mast cells.
Anesthetics, Local↗
G protein betagamma subunits induce stress fiber formation and focal adhesion assembly in a Rho-dependent manner in HeLa cells.
In fibroblasts, the G protein alpha subunits Galpha(12) and Galpha(13) stimulate Rho-dependent stress fiber formation and focal adhesion assembly, whereas G protein betagamma subunits instead exert a disruptive influence. We show here that the latter can, however, stimulate the formation of stress fibers and focal adhesions in epithelial-like HeLa cells. Transient expression of beta(1) with gamma(2), gamma(5), gamma(7), and gamma(12) in quiescent HeLa cells induced stress fiber formation and focal adhesion assembly as did expression of the constitutively active Galpha(12). Co-expression of betagamma with Galpha(i2) and the C-terminal fragment of the beta-adrenergic receptor kinase, both of which are known to bind and sequester free betagamma, blocked betagamma-induced stress fiber and focal adhesion formation. Inhibition was also noted with co-expression of a dominant negative mutant of Rho. Botulinum C3 exoenzyme, which ADP-ribosylates and inactivates Rho, and a Rho-associated protein kinase inhibitor, Y-27632, similarly inhibited betagamma-induced stress fiber and focal adhesion assembly. These results indicate that G protein betagamma subunits regulate Rho-dependent actin polymerization in HeLa cells.
3T3 Cells↗
Treatment of labial lentigos in atopic dermatitis with the frequency-doubled Q-switched Nd:YAG laser.
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Dermatitis, Atopic↗
Effects of gonadotropin-releasing hormone analog on expression of genes encoding the growth hormone/prolactin/somatolactin family and a pituitary-specific transcription factor in the pituitaries of prespawning sockeye salmon.
Gonadotropin-releasing hormone (GnRH) is a possible secretagogue of growth hormone (GH) and somatolactin (SL) in teleosts. Effects of GnRH on the levels of pituitary mRNAs encoding GH, prolactin (PRL), and SL were therefore examined in prespawning sockeye salmon (Oncorhynchus nerka). A capsule of GnRH analog (GnRHa) was implanted into the dorsal muscle of maturing sockeye salmon for 3 weeks. The levels of hormonal mRNAs were then determined by a quantitative dot blot analysis using single-stranded sense DNA of the same sequence of mRNA as the standard. Further, we analyzed effects of GnRHa on expression of the genes encoding pituitary-specific transcription factor (Pit-1/GHF-1). Relative levels of Pit-1/GHF-1 mRNAs were estimated by Northern blot analysis, which showed specific 2- and 3-kb bands of mRNAs. GnRHa significantly increased the level of SL mRNA in the males, but not in the females, compared to the control fish. It did not induce significant increases in the levels of GH and PRL mRNAs in both the males and the females. The levels of Pit-1/GHF-1 mRNAs in the control males tended to be higher than those in the initial controls, so that GnRHa might not be effective in enhancing expression of Pit-1/GHF-1 gene, except for the level of 3-kb Pit-1/GHF-1 mRNA in the females treated with 150 microg GnRHa. The pattern of changes in the levels of Pit-1/GHF-1 mRNAs were similar to those of GH and PRL mRNAs in both the males and the females and to that of SL mRNA in the females. These results indicate that, in prespawning sockeye salmon, GnRH can stimulate SL gene expression, but probably not through the Pit-1/GHF-1-dependent system.
Animals↗
Age-dependent changes in phenotypes and candidate gene analysis in a polygenic animal model of Type II diabetes mellitus; NSY mouse.
AIMS/HYPOTHESIS: The Nagoya-Shibata-Yasuda (NSY) mouse closely mimics human Type II (non-insulin-dependent) diabetes mellitus in that the onset is age-dependent, the animals are not severely obese, and both insulin resistance and impaired insulin response to glucose contribute to disease development. The aim of this study was to clarify the influence of age on the pathogenesis of diabetes and to analyse a candidate gene for Type II diabetes in this strain. METHODS: Several phenotypic characteristics related to diabetes mellitus were monitored longitudinally in male NSY and control C3H/He mice. The nucleotide sequence of Glut4, a candidate gene for Nidd1nsy (a susceptibility gene for Type II diabetes) on Chromosome 11, encoding insulin-sensitive glucose transporter, was determined in NSY and C3H mice. RESULTS: Glucose intolerance worsened with age, and fasting blood glucose and fasting plasma insulin concentration increased with age in NSY mice. Pancreatic insulin content increased until 24 weeks of age but then decreased at 48 weeks of age in NSY mice. The hypoglycaemic response to insulin was statistically significantly smaller in NSY than in C3H/He mice. The nucleotide sequence of GLUT4 cDNA was identical in NSY and C3H/He mice, but both were different from the sequence reported previously. CONCLUSION/INTERPRETATION: Insulin secretion and insulin resistance, as well as ageing possibly play an important part in the disease development in NSY mice. A decline of pancreatic insulin content in older age might cause the relative insulin deficiency in this strain. Nucleotide sequencing suggests that Glut4 is unlikely to be a candidate gene for Nidd1nsy.
3T3 Cells↗
Bilateral metachronous periosteal tibial amyloid tumors.
Localized primary periosteal amyloid tumors are extremely rare. A case of bilateral tibial amyloid tumor is presented. A 62-year-old woman initially presented with a painful mass in the anterior aspect of the right leg. There was no evidence of underlying systemic disease, including chronic infection or malignancy. Based on the results of resistance with Congo red staining to treatment with potassium permanganate and positivity for kappa light chain, we classified this particular case as AL-type amyloidosis. The patient noticed a swelling in the opposite leg 2 years later. The second tumor was also an AL-type amyloidoma. Amyloid tumors are generally solitary. This is the first case of bilateral periosteal amyloid tumors of the AL-type occurring in the tibiae.
Amyloidosis↗
Hyperpolarization is not responsible for the acetylcholine-induced negative chronotropic action in the presence of isoproterenol.
It has been reported that acetylcholine hyperpolarizes the maximum diastolic potential of canine Purkinje fibers through a pathway involving a G protein and induces a decrease in their automaticity. It is unclear, however, whether the negative chronotropic action of acetylcholine in the presence of beta-adrenergic stimulation is due to the hyperpolarization of the maximum diastolic potential or a decrease in the slope of phase 4 depolarization. We used standard microelectrode techniques to study the negative chronotropic mechanism of acetylcholine in the presence of isoproterenol in adult canine Purkinje fibers. Fibers were incubated for 24 hours in Tyrode's solution alone (n = 10) or plus pertussis toxin (n = 10), and then superfused with acetylcholine (10(-9) to 10(-4) M) in the presence of isoproterenol (10(-7) M). Acetylcholine in the presence of isoproterenol significantly decreased automaticity without hyperpolarization of the maximum diastolic potential, and decreased the slope of phase 4 depolarization. The effects of acetylcholine on automaticity and the slope of phase 4 depolarization were attenuated by pertussis toxin. The present findings indicate that the negative chronotropic action of acetylcholine in the presence of isoproterenol is due to the decrease in the slope of phase 4 depolarization through a pathway involving a pertussis toxin-sensitive G protein and that it is not the result of hyperpolarization of the maximum diastolic potential.
Acetylcholine↗
Histological study of articular cartilage in experimental rat knee arthritis induced by intracapsular injection of cationic polyethyleneimine.
Degeneration of proteoglycans and abnormalities in their metabolism have been assumed to be critical at an early stage of osteoarthritis. To clarify a trigger mechanism of osteoarthritis, anionic sites of knee articular cartilage were blocked by intracapsular injection of cationic polyethyleneimine of 2000 or 70,000 molecular weight (MW) into rat knee joints. Experimental or normal rats were examined by gross observation, roentgenography, cytokine interleukin-1beta (IL-1beta) assay, and light or electron microscopy. In both groups with the polyethyleneimine injection, the rats showed temporarily limping and swelling of their knee joints. By light or electron microscopic studies, knee articular cartilage was found to be degenerated at an early stage, but IL-1beta was within normal levels. At 2, 4, or 6 months, the deformity of the knee joints was obvious by roentgenography. Degeneration and hypofunction of proteoglycans might be related to the ultrastructural changes of articular cartilage at an early stage, though the inflammatory cytokine was not involved. At later stages the pathophysiology of the knee joints advanced chronically to typical osteoarthritis, which was more radically induced by the large molecular polyethyleneimine (70,000 MW). The functional impairment of anionic sites is a key point for elucidating the mechanism of osteoarthritic development in this animal model.
Animals↗
Paternal-maternal effects on phenotypic characteristics in spontaneously diabetic Nagoya-Shibata-Yasuda mice.
The Nagoya-Shibata-Yasuda (NSY) mouse is an inbred strain with spontaneous development of type 2 (non-insulin-dependent) diabetes mellitus. The purpose of this study was to determine the mode of inheritance of various phenotypes related to diabetes in this strain. Two reciprocal outcrosses, female C3H/He x male NSY F1 (C3NF1) and female NSY x male C3H/He F1 (NC3F1) mice, were performed. The phenotypic characteristics in both F1 mice were investigated. The cumulative incidence of diabetes was 100% (25 of 25) in male C3NF1 mice and 97% (29 of 30) in male NC3F1 mice at 48 weeks of age, indicating that diabetes in NSY mice was transmitted to male F1 hybrids in an autosomal dominant manner. Fatty liver also showed an autosomal dominant mode of inheritance. In contrast, epididymal fat accumulation and impaired insulin secretion showed an autosomal recessive mode of inheritance. The body mass index (BMI) showed a codominant mode of inheritance. Paternal-maternal effects associated with the severity of diabetes were observed. Insulin resistance was much more severe in male F1 mice than in the parental NSY strain. These data indicate different modes of inheritance among phenotypes related to type 2 diabetes. The presence of more severe insulin resistance in F1 mice versus the parental strains suggests the interaction of both parental genomes in the development of insulin resistance. The F1 mouse is expected to be useful for studies of the pathogenesis and genetic synergism of the insulin resistance syndrome.
Animals↗