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  • Influence of enteric helminths on the distribution of intestinal endocrine cells belonging to the diffuse endocrine system in brown trout, Salmo trutta L. 12962225

    The presence of intestinal helminths in the alimentary canal of brown trout, Salmo trutta L., can alter the number of cells that synthesize modulatory peptides. A total of 167 brown trout were collected from tributaries of the River Brenta (northern Italy), of which 119 (71.3%) specimens were infected with enteric helminths, 28 with the acanthocephalan Pomphorhynchus laevis Müller, 1776 with intensity of infection ranging from 1 to 162 (18.57 +/- 30.79) worms per host and 67 fish with the cestode Cyathocephalus truncatus Pallas, 1781. Intensity of infection with C. truncatus ranged from 1 to 85 (6.87 +/- 12.59) per fish. In 24 fish there were concurrent infections of both species of helminths. The caecal and middle regions of the intestine were the most heavily parasitized. Immunohistochemical tests showed a decrease in endocrine cells (ECs) of the diffuse endocrine system (DES) positive to gastrin, cholecystokinin-8, bombesin and secretin antisera in the intestine of the infected trout. The number of ECs immunoreactive to anti-glucagon serum did not show differences in the digestive tract of uninfected brown trout and in conspecifics parasitized with P. laevis. The density of cells containing glucagon-like material was low in the fish parasitized with C. truncatus. The results suggest that endoparasitic helminths induce alterations in the DES of infected S. trutta.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple

  • Purification and characterization of phosphoinositide 3-kinase from rat liver. 2174051

    Phosphoinositide 3-kinase was purified 27,000-fold from rat liver. The enzyme was purified by acid precipitation of the cytosol followed by chromatography on DEAE-Sepharose, S-Sepharose, hydroxylapatite, Mono-Q, and Mono-S columns. When analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the purified phosphoinositide 3-kinase preparation contained an 85-kDa protein and a protein doublet of approximately 110 kDa. The 85- and 110-kDa proteins focus together on native isoelectric focusing gels and are cross-linked by dithiobis(succinylamide propionate), showing that the 110- and 85-kDa proteins are a complex. The apparent size of the native enzyme, as determined by gel filtration, is 190 kDa. The 85-kDa subunit is the same protein previously shown to associate with polyoma virus middle T antigen and the platelet-derived growth factor receptor (Kaplan, D. R., Whitman, M., Schaffhausen, B., Pallas, D. C., White, M., Cantley, L., and Roberts, T. M. (1987) Cell 50, 1021-1029). The two proteins co-migrate on two-dimensional gels; and, using a Western blotting procedure, 32P-labeled middle T antigen specifically blots the 85-kDa protein. The purified enzyme phosphorylates phosphatidylinositol, phosphatidylinositol 4-phosphate, and phosphatidylinositol 4,5-bisphosphate. The apparent Km values for ATP were found to be 60 microM with phosphatidylinositol 4-phosphate or phosphatidylinositol 4,5-bisphosphate as the substrate. The apparent Km for phosphatidyinositol is 60 microM, for phosphatidylinositol 4-phosphate is 9 microM, and for phosphatidylinositol 4,5-bisphosphate is 4 microM. The maximum specific activity using phosphatidylinositol as the substrate is 0.8 mumol/mg/min. The enzyme requires Mg2+ with an optimum of 5 mM. Substitution of Mn2+ for Mg2+ results in only approximately 10% of the Mg2(+)-dependent activity. Physiological calcium concentrations have no effect on the enzyme activity. Phosphoinositide 3-kinase has a broad pH optimum around 7.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple

  • Cloning and characterization of a wortmannin-sensitive human phosphatidylinositol 4-kinase. 9020160

    Phosphatidylinositol (PtdIns) 4-kinases catalyze the synthesis of PtdIns-4-P, the immediate precursor of PtdIns-4,5-P2. Here we report the cloning of a novel, ubiquitously expressed PtdIns 4-kinase (PI4Kbeta). The 2.4-kilobase pair cDNA encodes a putative translation product of 801 amino acids which shows greatest homology to the yeast PIK1 gene. The recombinant protein exhibits lipid kinase activity when expressed in Escherichia coli, and specific antibodies recognize a 110-kDa PtdIns 4-kinase in cell lysates. The biochemical properties of PI4Kbeta are characteristic of a type III enzyme. Interestingly, both recombinant PI4Kbeta and the endogenous protein are inhibited by 150 nM wortmannin, suggesting that we have cloned the previously described PtdIns 4-kinase that is responsible for regulating the synthesis of agonist-sensitive pools of polyphosphoinositides (Nakanishi, S., Catt, J. K., and Balla, T. (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 5317-5321).
    Document Type:
    Reference
    Product Catalog Number:
    06-578

  • Lack of association between serum adiponectin levels and the Pro12Ala polymorphism in Asian Indians. 17335469

    AIMS: The aim of the study was to investigate the association of serum adiponectin levels with the Pro12Ala polymorphism of the peroxisome proliferator activated receptor-gamma (PPARG) gene in Asian Indians. METHODS: We selected 400 diabetic subjects, 200 with the Pro12Pro genotype (100 male and 100 female) and 200 with the Pro12Ala genotype (100 male and 100 female) and 400 age- and sex-matched normal glucose tolerance subjects with similar genotype profiles from the Chennai Urban Rural Epidemiology Study. Fasting serum adiponection levels were measured using radioimmunoassay. The Pro12Ala polymorphism was genotyped by PCR-restriction fragment length polymorphism using BstUI. RESULTS: All clinical and biochemical parameters were similar in the subjects with the Pro12Pro and Pro12Ala genotypes. There was no significant difference in serum adiponectin values between subjects with the Pro12Pro and Pro12Ala genotypes (males 5.4 vs. 5.8 microg/ml, P = 0.546; females 6.9 vs. 7.2 microg/ml, P = 0.748). Adiponectin values did not differ among these two genotypes even when categorized based on their diabetes status (normal glucose tolerance Pro12Pro 7.9 vs. Pro12Ala 7.7 microg/ml, P = 0.994; diabetes Pro12Pro 4.7 vs. Pro12Ala 5.4 microg/ml, P = 0.622). CONCLUSION: The Pro12Ala polymorphism of the PPARG gene is not associated with serum adiponectin levels in Asian Indians.
    Document Type:
    Reference
    Product Catalog Number:
    HADP-61HK
    Product Catalog Name:
    Human Adiponectin RIA

  • PHF8, a gene associated with cleft lip/palate and mental retardation, encodes for an N{varepsilon}-dimethyl lysine demethylase. 19843542

    Mutations of human PHF8 cluster within its JmjC encoding exons and are linked to mental retardation (MR) and a cleft lip/palate phenotype. Sequence comparisons, employing structural insights, suggest that PHF8 contains the double stranded beta-helix fold and ferrous iron binding residues that are present in 2-oxoglutarate-dependent oxygenases. We report that recombinant PHF8 is an Fe(II) and 2-oxoglutarate-dependent N(epsilon)-methyl lysine demethylase, which acts on histone substrates. PHF8 is selective in vitro for N(epsilon)-di- and mono-methylated lysine residues and does not accept trimethyl substrates. Clinically observed mutations to the PHF8 gene cluster in exons encoding for the double stranded beta-helix fold and will therefore disrupt catalytic activity. The PHF8 missense mutation c.836CT is associated with mild MR, mild dysmorphic features, and either unilateral or bilateral cleft lip and cleft palate in two male siblings. This mutant encodes a F279S variant of PHF8 that modifies a conserved hydrophobic region; assays with both peptides and intact histones reveal this variant to be catalytically inactive. The dependence of PHF8 activity on oxygen availability is interesting because the occurrence of fetal cleft lip has been demonstrated to increase with maternal hypoxia in mouse studies. Cleft lip and other congenital anomalies are also linked indirectly to maternal hypoxia in humans, including from maternal smoking and maternal anti-hypertensive treatment. Our results will enable further studies aimed at defining the molecular links between developmental changes in histone methylation status, congenital disorders and MR.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Cytochemical identification of programmed cell death in the fusing fetal mouse palate by specific labelling of DNA fragmentation. 7527193

    The process of palate fusion was examined in 13- and 14-day-old mouse fetuses by using in situ staining for nuclear DNA fragmentation (TUNEL method) and immunofluorescent staining for keratin, with special reference to the disruption of the midline epithelial seam. TUNEL-positive cells were found in the disappearing midline seam and the oral and nasal epithelial triangles at some late stages of palate fusion, but not in the palatal shelves prior to contact or in the intact midline epithelial seam. It seems that DNA fragmentation or apoptosis is required for the midline epithelial seam to disrupt, but may not be necessary for initial contact of palatal shelves or for the epithelial fusion of opposing palatal shelves. A similar sign of apoptotic cell death was observed in the disappearing epithelial seam between the fusing nasal septum and dorsal palate. We have demonstrated that apoptotic programmed cell death does occur at some stages of palate fusion, although the present results do not exclude the possibility of epithelial-mesenchymal transformation and the oral and nasal migration of midline epithelial cells.
    Document Type:
    Reference
    Product Catalog Number:
    17-141

  • Helicobacter pylori in the palatine tonsils of patients with IgA nephropathy compared with those of patients with recurrent pharyngotonsillitis. 17714758

    Helicobacter pylori infection is acquired by oral ingestion. However, the morphology and microscopic localization of H pylori in the human oral cavity and pharynx are unknown. In the present study, we performed immunohistochemistry, immunoelectron microscopy, in situ hybridization, and polymerase chain reaction to identify H pylori in the palatine tonsils of 32 patients with immunoglobulin A nephropathy (IgAN) and 141 patients with recurrent pharyngotonsillitis (RPT). H pylori in coccoid form was present in bacterial colonies and horny layers of the stratified squamous epithelium in tonsillar crypts. We described for the first time the morphology of H pylori in palatine tonsils. Most bacterial colonies were sulfur granules with Actinomyces israelii (A israelii), and A israelii showed significant coexistence with H pylori (P=.011). The prevalence of H pylori in palatine tonsils of the RPT group increased steeply with age, but one fourth of the patients were found not to have tonsillar H pylori in adulthood. All patients with IgAN had H pylori in palatine tonsils. The prevalence of H pylori was greater in the IgAN group than in the RPT group, and the difference was statistically significant (P.001). In contrast, A israelii was unrelated to age and clinical diagnosis (P=.722). In conclusion, our results demonstrate that H pylori in coccoid form is present in palatine tonsils and may indicate that H pylori in palatine tonsils is among the antigens causative of IgAN.
    Document Type:
    Reference
    Product Catalog Number:
    MAB3412
    Product Catalog Name:
    Anti-Cytokeratin AE1/AE3 Antibody, recognizes acidic & basic cytokeratins, clone AE1/AE3

  • MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis. 18264099

    Disruption of signaling pathways such as those mediated by sonic hedgehog (Shh) or platelet-derived growth factor (Pdgf) causes craniofacial abnormalities, including cleft palate. The role that microRNAs play in modulating palatogenesis, however, is completely unknown. We show that, in zebrafish, the microRNA Mirn140 negatively regulates Pdgf signaling during palatal development, and we provide a mechanism for how disruption of Pdgf signaling causes palatal clefting. The pdgf receptor alpha (pdgfra) 3' UTR contained a Mirn140 binding site functioning in the negative regulation of Pdgfra protein levels in vivo. pdgfra mutants and Mirn140-injected embryos shared a range of facial defects, including clefting of the crest-derived cartilages that develop in the roof of the larval mouth. Concomitantly, the oral ectoderm beneath where these cartilages develop lost pitx2 and shha expression. Mirn140 modulated Pdgf-mediated attraction of cranial neural crest cells to the oral ectoderm, where crest-derived signals were necessary for oral ectodermal gene expression. Mirn140 loss of function elevated Pdgfra protein levels, altered palatal shape and caused neural crest cells to accumulate around the optic stalk, a source of the ligand Pdgfaa. These results suggest that the conserved regulatory interactions of mirn140 and pdgfra define an ancient mechanism of palatogenesis, and they provide candidate genes for cleft palate.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • How does immune challenge inhibit ingestion of palatable food? Evidence that systemic lipopolysaccharide treatment modulates key nodal points of feeding neurocircuitry. 18562160

    Immune challenge induces behavioral changes including reduced ingestion of palatable food. Multiple pathways likely contribute to this effect, including viscerosensory pathways controlling hypothalamic feeding circuits or by influence on "reward" circuitry previously established to control ingestive behavior. To investigate whether the effects of immune challenge may influence this network, we compared brain activation patterns in animals trained to drink a palatable sweetened milk solution and treated systemically with either the immune stimulant lipopolysaccharide (LPS) or saline. Brain sections were processed for localization of the activation marker c-Fos in neurons of regions implicated in regulation of feeding behavior. Sweetened milk ingestion was associated with increased numbers of c-Fos positive neurons in the caudal core and shell of the nucleus accumbens (NAc), the paraventricular thalamus (PVT), central nucleus of the amygdala (CEA), the basal lateral amygdala (BLA), in orexin-A containing neurons of the lateral hypothalamus (LH), and in cocaine and amphetamine regulated transcript (CART) neurons of the arcuate hypothalamus. In LPS-treated animals sweetened milk consumption was significantly reduced, as was c-Fos induction in the hypothalamic orexin-A and CART neurons, and in the BLA. In addition, induction of c-Fos in the rostral regions of the NAc, the PVT, and CEA was increased following LPS treatment, compared to controls. The findings from this study point to a network of brain regions (LH, PVT, NAc, and BLA) previously implicated in the modulation of feeding behavior, reward, and arousal that may also contribute to neural substrates involved in the reorganization of behavioral priorities that occurs during sickness.
    Document Type:
    Reference
    Product Catalog Number:
    AB3704
    Product Catalog Name:
    Anti-Orexin-A Antibody

  • Cell proliferation and apoptosis in the fusion of human primary and secondary palates. 22813218

    The markers of cell proliferation (Ki-67) and apoptosis [caspase-3, TdT-mediated biotin-dUTP nick-end labelling (TUNEL)] and the expression of syndecan-1 and heat shock protein 70 (Hsp70) were analyzed immunohistochemically in 11 developing human palates, from developmental weeks 6 to 10. During fusion of the primary palate, the proportion of proliferating cells decreased from 42 to 32% and the proportion of apoptotic cells decreased from 11 to 7% in the medial-edge epithelium. At later stages, the proportions of both types of cells decreased in the ectomesenchyme, except for proliferating cells in its non-condensing part. At developmental weeks 9-10, the epithelial seam in the secondary palate comprised 28% proliferative cells and 5% apoptotic cells. While condensing ectomesenchyme contained more apoptotic cells than proliferating cells, the opposite was observed for the non-condensing ectomesenchyme. Co-expression of syndecan-1 and Hsp70 was detected in cells budding from the epithelial seam. Our study indicates similar principles for human primary palate and secondary palate fusion, and parallel persistence of proliferation and apoptotic activity. While proliferation enables growth and fusion of different palatal primordia, apoptosis results in the removal of of large numbers epithelial cells at the fusion point. The disintegration of seam remnants seems to be executed through the processes of change in protein content and cell migration, probably leading to cell death as their final outcome.
    Document Type:
    Reference
    Product Catalog Number:
    AP132F
    Product Catalog Name:
    Goat Anti-Rabbit IgG Antibody, FITC conjugate