Home  About us  Contact
 

Hybridization Study (hybridization + study)

Distribution by Scientific Domains
Medical Sciences66%
Life Sciences33%

Kinds of Hybridization Study

  • situ hybridization study
    		•

    Selected Abstracts

    Upregulation of [3H]methyllycaconitine binding sites following continuous infusion of nicotine, without changes of ,7 or ,6 subunit mRNA: an autoradiography and in situ hybridization study in rat brain

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2002
    Manolo Mugnaini
    Abstract It is well established that exposure of experimental animals to nicotine results in upregulation of the ,4,2-subtype of neuronal nicotinic acetylcholine receptors (nAChRs). The aim of this study was to determine the effect of nicotine on the levels of ,7-nAChRs in rat brain, for which only partial information is available. Rats were infused with nicotine (3 mg/kg/day) or saline for 2 weeks and their brains processed for receptor autoradiography with [3H]methyllycaconitine (MLA), a radioligand with nanomolar affinity for ,7-nAChRs. In control rats binding was high in hippocampus, intermediate in cerebral cortex and hypothalamus, and low in striatum, thalamus and cerebellum. There was high correlation between the distribution of [3H]MLA binding sites and ,7 subunit mRNA (r = 0.816). With respect to saline-treated controls, nicotine-treated rats presented higher [3H]nicotine binding in 11 out of 15 brain regions analysed (average increase 46 ± 6%). In contrast, only four regions showed greater [3H]MLA binding, among which the ventral tegmental area (VTA) and cingulate cortex (mean increase 32 ± 3%). No changes in ,7 mRNA levels were observed after nicotine treatment. Similarly, there was no variation of ,6 subunit transcript in the VTA, a region which may contain MLA-sensitive (non-,7)-,6*-nAChRs (Klink et al., 2001). In conclusion, nicotine increased [3H]MLA binding, although to a smaller extent and in a more restricted regional pattern than [3H]nicotine. The enhancement of binding was not paralleled by a significant change of ,7 and ,6 subunit transcription. Finally, the present results provide the first anatomical description of the distribution of [3H]MLA binding sites in rat brain. [source]

    MLL/SEPTIN6 chimeric transcript from inv ins(X;11)(q24;q23q13) in acute monocytic leukemia: Report of a case and review of the literature

    GENES, CHROMOSOMES AND CANCER, Issue 1 2003
    Hee-Jin Kim
    Rearrangements of the MLL gene on chromosome 11, band q23, are one of the most common genetic changes in acute leukemia. Reciprocal translocation is the most common form of MLL rearrangement, and the partner genes in MLL translocation are notably diverse. Involvement of the SEPTIN6 gene on Xq24 in MLL rearrangements occurs very rarely, with only six cases having been documented in the literature. Of note, the MLL/SEPTIN6 rearrangements in these cases were cryptic or complex, and it was shown that the 5,- MLL/SEPTIN6 -3, transcript resides on the derivative X chromosome rather than on the derivative chromosome 11 as in the majority of cases of MLL translocations. These observations suggested that MLL and SEPTIN6 reside on their respective chromosome loci in reverse orientation, that is, centromere-to-telomere and telomere-to-centromere, respectively. We here report a case of acute monocytic leukemia with inv ins(X;11)(q24;q23q13) in a 29-month-old child. Fluorescence in situ hybridization study revealed the break-apart 5,- MLL segment to be translocated to the derivative X chromosome, and reverse transcriptase,polymerase chain reaction followed by sequencing analysis confirmed the 5,- MLL/SEPTIN6 -3, chimeric transcript. This case is the first to provide direct cytogenetic evidence for the salient nature of the MLL/SEPTIN6 rearrangement. We reviewed clinical and cytogenetic features of all cases of 11q23 and Xq22,24 rearrangements reported up to now, including six cases where the involvement of the SEPTIN6 gene was confirmed by molecular techniques. © 2003 Wiley-Liss, Inc. [source]

    Transgenic mouse lines expressing synaptopHluorin in hippocampus and cerebellar cortex

    GENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2005
    Rikita Araki
    Abstract We generated six transgenic mouse lines in which synaptopHluorin (SpH), one of green fluorescent protein-based sensors of vesicular exocytosis, was expressed under the control of neuron-specific Thy-1.2 promoter. In situ hybridization study revealed that SpH mRNA was expressed in a broad spectrum of brain regions in four of them, whereas in others it was expressed in the specific regions of the hippocampus. In one particular line, SpH immunoreactivity was specifically observed in the mossy fiber presynaptic terminals of both hippocampus and cerebellar cortex. The fluorescence intensity of these presynaptic terminals was somewhat decreased by acidic buffer superfusion and greatly increased by vesicular neutralization of pH, indicating that the SpH molecules are mainly distributed in the synaptic vesicles. The exocytosis-dependent fluorescence increment was measured upon activation of a single presynaptic terminal. These transgenic lines are expected to facilitate morphological and physiological studies of presynaptic terminals in a variety of regions of the brain. genesis 42:53,60, 2005. © 2005 Wiley-Liss, Inc. [source]

    Immunohistochemical expression of 14-3-3 sigma protein in various histological subtypes of uterine cervical cancers

    PATHOLOGY INTERNATIONAL, Issue 10 2004
    Takaaki Sano
    14-3-3 sigma (,) has been a major G2/M checkpoint control gene and has demonstrated that its inactivation in various cancers occurs mostly by epigenetic hypermethylation, not by genetic change. In order to confirm 14-3-3, protein expression together with p16 and p53 in cervical cancers, immunohistochemistry was performed using various histological subtypes of cervical cancers and dysplasia. Strong and diffuse immunoreactivity for 14-3-3, was uniformly observed in all the cervical dysplasia (17/17) and squamous cell carcinomas (29/29) including human papillomavirus (HPV)-negative cases. Even in adenosquamous carcinomas and adenocarcinomas of the cervix, immunohistochemical expression of 14-3-3, was shown with relatively high frequency (13/15, 87% and 22/27, 81%). In the in situ hybridization study, mRNA of 14-3-3, was expressed in six of eight immunohistochemical-negative cases. Therefore, the undetectable expression of 14-3-3, protein in cervical cancers might, at least in part, be due to a proteolysis not epigenetic hypermethylation. It is of interest that cancers without 14-3-3, expression were predominantly those lacking HPV DNA, and that there were no cases with concomitant inactivation of 14-3-3, and p16 in the present study. These observations are consistent with the hypothesis that inactivation of either 14-3-3, or p16 has an effect equivalent to the expression of E6 and E7 oncoproteins of HPV. [source]

    DNA copy number changes in carcinoma in pleomorphic adenoma of the salivary gland: A comparative genomic hybridization study

    PATHOLOGY INTERNATIONAL, Issue 8 2002
    Takashi Morio
    Pleomorphic adenoma is the most common benign tumor of the salivary glands and is rarely associated with concurrent epithelial malignancy, which is designated as carcinoma in pleomorphic adenoma (CPA). Genetic abnormalities potentially related to the development of CPA have not been fully investigated. We analyzed DNA copy number changes in each of the adenomatous and carcinomatous components of seven CPA by comparative genomic hybridization using DNA extracted from microdissected tissues of formalin-fixed, paraffin-embedded tumor samples. Carcinomatous components of CPA showed multiple DNA copy number changes at 1,18 different genomic sites (mean 13 sites). Adenomatous components displayed less frequent DNA copy number changes (0,13 sites; mean, 5). In both components, the majority of the changes were gains. The most common recurrent gains in carcinomatous components were seen at 6q (four cases in each), whereas gains at 13q1,2 and 15q1 were most frequently detected in adenomatous components (three cases in each). In five CPA, the same chromosomal regions were involved in the DNA copy number changes detected in both components. Our data suggest that an accumulated or increased number of chromosomal changes including 6q abnormalities may be associated with the development of carcinomatous components in a subset of CPA. [source]

    Decreased GAD65 mRNA levels in select subpopulations of neurons in the cerebellar dentate nuclei in autism: an in situ hybridization study

    AUTISM RESEARCH, Issue 1 2009
    Jane Yip
    Abstract The laterally positioned dentate nuclei lie in a key position in the cerebellum to receive input from Purkinje cells in the lateral cerebellar hemisphere participating in both motor and cognitive functions. Although neuropathology of the four cerebellar nuclei using Nissl staining has been qualitatively reported in children and adults with autism, surprisingly the dentate nuclei appeared less affected despite reported reductions in Purkinje cells in the posterolateral cerebellar hemisphere. To determine any underlying abnormalities in the critically important GABAergic system, the rate-limiting GABA synthesizing enzyme, glutamic acid decarboxylase (GAD) type 65 was measured via in situ hybridization histochemistry in dentate somata. GAD65 mRNA labeling revealed two distinct subpopulations of neurons in adult control and autism postmortem brains: small-sized cells (about 10,12,µm in diameter, presumed interneurons) and larger-sized neurons (about 18,20,µm in diameter, likely feedback to inferior olivary neurons). A mean 51% reduction in GAD65 mRNA levels was found in the larger labeled cells in the autistic group compared with the control group (P=0.009; independent t -test) but not in the smaller cell subpopulation. This suggests a disturbance in the intrinsic cerebellar circuitry in the autism group potentially interfering with the synchronous firing of inferior olivary neurons, and the timing of Purkinje cell firing and inputs to the dentate nuclei. Disturbances in critical neural substrates within these key circuits could disrupt afferents to motor and/or cognitive cerebral association areas in the autistic brain likely contributing to the marked behavioral consequences characteristic of autism. [source]