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  • Neurochemical phenotype of vagal afferent neurons activated to express C-FOS in response to luminal stimulation in the rat. 15590158

    The vagus nerve conveys meal-induced primary afferent responses to the brainstem. Electrophysiological studies indicate that luminal stimuli such as osmolarity and the digestion products of carbohydrates elicit powerful vagal nodose neuronal responses by activating serotonin 3 (5-hydroxytryptamine-3, 5-HT3) receptors on intestinal mucosal afferent fibers. To characterize the neurochemical phenotype of neurotransmitters in vagal nodose neurons that are activated by luminal stimulation, we examined c-fos protein (c-Fos) expression in response to luminal stimulation in conscious rats. A double-labeling technique using antisera to glutamate (Glu), substance P (SP), calcitonin gene-related peptide (CGRP), and somatostatin (SS) was used to determine the neurochemical profile of c-Fos-positive neurons. c-Fos immunoreactivity was insignificant in vehicle-treated rats. Luminal perfusions of NaCl (500 mOsm), tap water (5 mOsm), maltose (300 mmol/l), and 5-HT (10(-5) mol/l) each elicited a significant increase in the number of cells expressing c-Fos. Chronic vagotomy eliminated an increase in nodose neuronal c-Fos expression, and the 5-HT3 receptor antagonist granisetron significantly reduced it. Glu-, SP-, and CGRP-containing neurons represented 28%, 53%, and 19%, respectively, of the total population of nodose neurons. Few neurons contained SS. Double-labeling studies revealed that of the c-Fos-positive neurons responsive to hypertonic NaCl, 52%, 41%, and 3% exhibited immunoreactivity for Glu, SP, and CGRP, respectively. Of those responsive to tap water, 47%, 50%, and 4% exhibited immunoreactivity for Glu-, SP- and CGRP, respectively. In addition, 44%, 38%, and 8% of 5-HT-stimulated and 30%, 32%, and 5% of maltose-stimulated c-Fos-positive neurons exhibited, respectively, Glu, SP, and CGRP immunoreactivity. The few neurons that contained SS did not express c-Fos. CONCLUSIONS: Vagal primary afferent neurons that respond to 5-HT-dependent luminal stimuli, such as hyperosmolarity and maltose, contain mainly Glu and SP. These neurons appear to play an important role in the mediation of the vago-vagal reflex elicited by luminal stimuli.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • De novo generation of satellite DNA-based artificial chromosomes by induced large-scale amplification. 21431723

    Mammalian artificial chromosomes (MACs) are engineered chromosomes with defined genetic content that can function as non-integrating vectors with large carrying capacity and stability. The large carrying capacity allows the engineering of MACs with multiple copies of the same transgene, gene complexes, and to include regulatory elements necessary for the regulated expression of transgene(s). In recent years, different approaches have been explored to generate MACs (Vos Curr Opin Genet Dev 8:351-359, 1998; Danielle et al. Trends Biotech 23:573-583, 2005; Duncan and Hadlaczky Curr Opin Biotech 18:420-424, 2007): (1) the de novo formation by centromere seeding, the bottom-up approach, (2) the truncation of natural chromosomes or the modification of naturally occurring minichromosomes, the top-down approach, and (3) the in vivo inductive approach. Satellite DNA-based artificial chromosomes (SATACs) generated by the in vivo inductive method have the potential to become an efficient tool in diverse gene technology applications such as cellular protein manufacturing (Kennard et al. BioPharm Int 20:52-59, 2007; Kennard et al. Biotechnol Bioeng 104:526-539, 2009; Kennard et al. Biotechnol Bioeng 104:540-553, 2009), transgenic animal production (Telenius et al. Chromosome Res 7:3-7, 1999; Co et al. Chromosome Res 8:183-191, 2000; Monteith et al. Methods Mol Biol 240:227-242, 2003), and ultimately a safe vector for gene therapy (Vanderbyl et al. Stem Cells 22:324-333, 2004; Vanderbyl et al. Exp Hematol 33:1470-1476, 2005; Katona et al. Cell. Mol. Life Sci 65:3830-3838, 2008). A detailed protocol for the de novo generation of satellite DNA-based artificial chromosomes (SATACs) via induced large-scale amplification is presented.
    Document Type:
    Reference
    Product Catalog Number:
    AQ300D

  • Impairment of retrograde neuronal transport in oxaliplatin-induced neuropathy demonstrated by molecular imaging. 23029238

    The purpose of our study was to utilize a molecular imaging technology based on the retrograde axonal transport mechanism (neurography), to determine if oxaliplatin-induced neurotoxicity affects retrograde axonal transport in an animal model.Mice (n = 8/group) were injected with a cumulative dose of 30 mg/kg oxaliplatin (sufficient to induce neurotoxicity) or dextrose control injections. Intramuscular injections of Tetanus Toxin C-fragment (TTc) labeled with Alexa 790 fluorescent dye were done (15 ug/20 uL) in the left calf muscles, and in vivo fluorescent imaging performed (0-60 min) at baseline, and then weekly for 5 weeks, followed by 2-weekly imaging out to 9 weeks. Tissues were harvested for immunohistochemical analysis.With sham treatment, TTc transport causes fluorescent signal intensity over the thoracic spine to increase from 0 to 60 minutes after injection. On average, fluorescence signal increased 722%+/-117% (Mean+/-SD) from 0 to 60 minutes. Oxaliplatin treated animals had comparable transport at baseline (787%+/-140%), but transport rapidly decreased through the course of the study, falling to 363%+/-88%, 269%+/-96%, 191%+/-58%, 121%+/-39%, 75%+/-21% with each successive week and stabilizing around 57% (+/-15%) at 7 weeks. Statistically significant divergence occurred at approximately 3 weeks (p≤0.05, linear mixed-effects regression model). Quantitative immuno-fluorescence histology with a constant cutoff threshold showed reduced TTc in the spinal cord at 7 weeks for treated animals versus controls (5.2 Arbitrary Units +/-0.52 vs 7.1 AU +/-1.38, pless than 0.0004, T-test). There was no significant difference in neural cell mass between the two groups as shown with NeuN staining (10.2+/-1.21 vs 10.5 AU +/-1.53, pgreater than 0.56, T-test).We show-for the first time to our knowledge-that neurographic in vivo molecular imaging can demonstrate imaging changes in a model of oxaliplatin-induced neuropathy. Impaired retrograde neural transport is suggested to be an important part of the pathophysiology of oxaliplatin-induced neuropathy.
    Document Type:
    Reference
    Product Catalog Number:
    MAB377X
    Product Catalog Name:
    Anti-NeuN Antibody, clone A60, Alexa Fluor®488 conjugated

  • Mannitol-facilitated CNS entry of rAAV2 vector significantly delayed the neurological disease progression in MPS IIIB mice. 19587708

    The presence of the blood-brain barrier (BBB) presents the most critical challenge in therapeutic development for mucopolysaccharidosis (MPS) IIIB, a lysosomal storage disease with severe neurological manifestation, because of alpha-N-acetylglucosaminidase (NaGlu) deficiency. Earlier, we showed a global central nervous system (CNS) transduction in mice by mannitol-facilitated entry of intravenous (IV)-delivered recombinant adeno-associated viral serotype 2 (rAAV2) vector. In this study, we optimized the approach and showed that the maximal transduction in the CNS occurred when the rAAV2 vector was IV injected at 8 min after mannitol administration, and was approximately 10-fold more efficient than IV delivery of the vector at 5 or 10 min after mannitol infusion. Using this optimal (8 min) regimen, a single IV infusion of rAAV2-CMV-hNaGlu vector is therapeutically beneficial for treating the CNS disease of MPS IIIB in adult mice, with significantly extended survival, improved behavioral performance, and reduction of brain lysosomal storage pathology. The therapeutic benefit correlated with maximal delivery to the CNS, but not peripheral tissues. This milestone data shows the first effective gene delivery across the BBB to treat CNS disease. The critical timing of vector delivery and mannitol infusion highlights the important contribution of this pretreatment to successful intervention, and the long history of safe use of mannitol in patients bodes well for its application in CNS gene therapy.
    Document Type:
    Reference
    Product Catalog Number:
    MAB360
    Product Catalog Name:
    Anti-Glial Fibrillary Acidic Protein Antibody, clone GA5

  • High XRCC1 protein expression is associated with poorer survival in patients with head and neck squamous cell carcinoma. 21908577

    We evaluated X-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1) protein in head and neck squamous cell carcinoma (HNSCC) patients in association with outcome.XRCC1 protein expression was assessed by immunohistochemical (IHC) staining of pretreatment tissue samples in 138 consecutive HNSCC patients treated with surgery (n = 31), radiation (15), surgery and radiation (23), surgery and adjuvant chemoradiation (17), primary chemoradiation (51), and palliative measures (1).Patients with high XRCC1 expression by IHC (n = 77) compared with patients with low XRCC1 expression (n = 60) had poorer median overall survival (OS; 41.0 months vs. OS not reached, P = 0.009) and poorer progression-free survival (28.0 months vs. 73.0 months, P = 0.031). This association was primarily due to patients who received chemoradiation (median OS of high- and low-XRCC1 expression patients, 35.5 months and not reached respectively, HR 3.48; 95% CI: 1.44-8.38; P = 0.006). In patients treated with nonchemoradiation modalities, there was no survival difference by XRCC1 expression. In multivariable analysis, high XRCC1 expression and p16(INK4a)-positive status were independently associated with survival in the overall study population (HR = 2.62; 95% CI: 1.52-4.52; P less than 0.001 and HR = 0.21; 95% CI: 0.06-0.71; P = 0.012, respectively) and among chemoradiation patients (HR = 6.02; 95% CI: 2.36-15.37; P less than 0.001 and HR = 0.26; 95% CI: 0.08-0.92, respectively; P = 0.037).In HNSCC, high XRCC1 protein expression is associated with poorer survival, particularly in patients receiving chemoradiation. Future validation of these findings may enable identification of HNSCC expressing patients who benefit from chemoradiation treatment.
    Document Type:
    Reference
    Product Catalog Number:
    MAB4133
    Product Catalog Name:
    Anti-p16 Antibody, clone D25

  • Exaggerated natriuresis during clamping of systemic NO supply in healthy young men. 21749320

    NO (nitric oxide) may be involved in fluid homoeostasis. We hypothesized that increases in NO synthesis contribute to acute, saline-induced natriuresis, which, therefore, should be blunted when NO availability is stabilized. Young men were studied during simultaneous infusions of L-NAME [NG-nitro-L-arginine methyl ester; bolus of 750 μg·kg⁻¹ of body weight and 8.3 μg·min⁻¹·kg⁻¹ of body weight] and SNP (sodium nitroprusside), the latter at a rate preventing L-NAME from increasing total peripheral resistance ('NO-clamping'). Slow volume expansion (saline, 20 μmol of NaCl·min⁻¹·kg⁻¹ of body weight for 3 h) was performed with and without concomitant NO-clamping. NO-clamping itself decreased RPF (renal plasma flow; P~0.02) and tended to decrease arterial blood pressure [MABP (mean arterial blood pressure)]. Volume expansion markedly decreased the plasma levels of renin, AngII (angiotensin II) and aldosterone (all Pless than 0.001), while MABP (oscillometry), heart rate, cardiac output (impedance cardiography), RPF (by p-aminohippurate), GFR [glomerular filtration rate; by using 51Cr-labelled EDTA] and plasma [Na+] and [K+] remained constant. Volume expansion increased sodium excretion (Pless than 0.02) at constant filtered load, but more so during NO-clamping than during control (+184% compared with 52%; Pless than 0.0001). Urinary nitrate/nitrite excretion increased during volume expansion; plasma cGMP and plasma vasopressin were unchanged. The results demonstrate that NO-clamping augments sodium excretion in response to volume expansion at constant MABP and GFR, reduced RPF and decreased renin system activity, a response termed hypernatriuresis. The results indicate that mediator(s) other than MABP, RPF, GFR and renin system activity contribute significantly to the homoeostatic response to saline loading, but the specific mechanisms of hypernatriuresis remain obscure.
    Document Type:
    Reference
    Product Catalog Number:
    AB3096
    Product Catalog Name:
    Anti-Orexin Antibody, Prepro

  • Role of mesenchymal stem cells in osteosarcoma and metabolic reprogramming of tumor cells. 25277190

    The tumor microenvironment plays an important role in cancer progression. Here, we focused on the role of reactive mesenchymal stem cells (MSC) in osteosarcoma (OS), and used human adipose MSC and a panel of OS cell lines (Saos-2, HOS, and 143B) to investigate the mutual effect of normal-cancer cell metabolic programming. Our results showed that MSC are driven by oxidative stress induced by OS cells to undergo Warburg metabolism, with increased lactate production. Therefore, we analyzed the expression of lactate monocarboxylate transporters. By real time PCR and immunofluorescence, in MSC we detected the expression of MCT-4, the transporter for lactate efflux, whereas MCT-1, responsible for lactate uptake, was expressed in OS cells. In agreement, silencing of MCT-1 by siRNA significantly affected the ATP production in OS cancer cells. Thus, cancer cells directly increase their mitochondrial biogenesis using this energy-rich metabolite that is abundantly provided by MSC as an effect of the altered microenvironmental conditions induced by OS cells. We also showed that lactate produced by MSC promotes the migratory ability of OS cells. These data provide novel information to be exploited for cancer therapies targeting the mutual metabolic reprogramming of cancer cells and their stroma.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1273
    Product Catalog Name:
    Anti-Mitochondria Antibody, surface of intact mitochondria, clone 113-1

  • Somatostatin receptor subtype 2 in high-grade gliomas: PET/CT with (68)Ga-DOTA-peptides, correlation to prognostic markers, and implications for targeted radiotherapy. 25977882

    High-grade gliomas (HGGs) express somatostatin receptors (SSTR), rendering them candidates for peptide receptor radionuclide therapy (PRRT). Our purpose was to evaluate the potential of (68)Ga-DOTA-1-Nal(3)-octreotide ((68)Ga-DOTANOC) or (68)Ga-DOTA-Tyr(3)-octreotide ((68)Ga-DOTATOC) to target SSTR subtype 2 (SSTR2) in HGGs, and to study the association between SSTR2 expression and established biomarkers.Twenty-seven patients (mean age 52 years) with primary or recurrent HGG prospectively underwent (68)Ga-DOTA-peptide positron emission tomography/computed tomography (PET/CT) before resection. Maximum standardized uptake values (SUVmax) and receptor binding potential (BP) were calculated on PET/CT and disruption of blood-brain barrier (BBB) from contrast-enhanced T1-weighted magnetic resonance imaging (MRI-T1-Gad). Tumor volume concordance between PET and MRI-T1-Gad was assessed by Dice similarity coefficient (DC) and correlation by Spearman's rank. Immunohistochemically determined SSTR2 status was compared to receptor imaging findings, prognostic biomarkers, and survival with Kruskal-Wallis, Pearson chi-square, and multivariate Cox regression, respectively.All 19 HGGs with disrupted BBB demonstrated tracer uptake. Tumor SUVmax (2.25 ± 1.33) correlated with MRI-T1-Gad (r = 0.713, P = 0.001) although DC 0.41 ± 0.19 suggested limited concordance. SSTR2 immunohistochemistry was regarded as positive in nine HGGs (32%) but no correlation with SUVmax or BP was found. By contrast, SSTR2 expression was associated with IDH1 mutation (P = 0.007), oligodendroglioma component (P = 0.010), lower grade (P = 0.005), absence of EGFR amplification (P = 0.021), and longer progression-free survival (HR 0.161, CI 0.037 to 0.704, P = 0.015).In HGGs, uptake of (68)Ga-DOTA-peptides is associated with disrupted BBB and cannot be predicted by SSTR2 immunohistochemistry. Thus, PET/CT shows limited value to detect HGGs suitable for PRRT. However, high SSTR2 expression portends favorable outcome along with established biomarkers such as IDH1 mutation.ClinicalTrials.gov NCT01460706.
    Document Type:
    Reference
    Product Catalog Number:
    AB5681

  • Two gamma interferon-activated site-like elements in the human cytomegalovirus major immediate-early promoter/enhancer are important for viral replication. 15795289

    Human cytomegalovirus (HCMV) infection directly initiates a signal transduction pathway that leads to activation of a large number of cellular interferon-stimulated genes (ISGs). Our previous studies demonstrated that two interferon response elements, the interferon-stimulated response element and gamma interferon-activated site (GAS), in the ISG promoters serve as HCMV response sites (VRS). Interestingly, two GAS-like VRS elements (VRS1) were also present in the HCMV major immediate-early promoter-enhancer (MIEP/E). In this study, the importance of these VRS elements in viral replication was investigated. We demonstrate that the expression of the major IE genes, IE1 and IE2, is interferon inducible. To understand the biological significance of this signal transduction pathway in HCMV major IE expression, the two VRS1 in the MIEP/E were mutated. Mutant HCMVs in which the VRS elements were deleted or that contained point mutations grew dramatically more slowly than wild-type virus at a low multiplicity of infection (MOI). Insertion of wild-type VRS1 into the mutant viral genome rescued the slow growth phenotype. Furthermore, the expression levels of major IE RNAs and proteins were greatly reduced during infection with the VRS mutants at a low MOI. HCMV microarray analysis indicated that infection of host cells with the VRS mutant virus resulted in a global reduction in the expression of viral genes. Collectively, these data demonstrate that the two VRS elements in the MIEP/E are necessary for efficient viral gene expression and replication. This study suggests that although the HCMV-initiated signal transduction pathway results in induction of cellular antiviral genes, it also functions to stimulate viral major IE gene expression. This might be a new viral strategy in which the pathway is used to regulate gene expression and play a role in reactivation.
    Document Type:
    Reference
    Product Catalog Number:
    MAB810

  • AMSH is required to degrade ubiquitinated proteins in the central nervous system. 21531206

    Deubiquitination is a biochemical process that mediates the removal of ubiquitin moieties from ubiquitin-conjugated substrates. AMSH (associated molecule with the SH3 domain of STAM) is a deubiquitination enzyme that participates in the endosomal sorting of several cell-surface molecules. AMSH impairment results in missorted ubiquitinated cargoes in vitro and severe neurodegeneration in vivo, but it is not known how AMSH deficiency causes neuronal damage in the brain. Here, we demonstrate that AMSH(-/-) mice developed ubiquitinated protein accumulations as early as embryonic day 10 (E10), and that severe deposits were present in the brain at postnatal day 8 (P8) and P18. Interestingly, TDP-43 was found to accumulate and colocalize with glial marker-positive cells in the brain. Glutamate receptor and p62 accumulations were also found; these molecules colocalized with ubiquitinated aggregates in the brain. These data suggest that AMSH plays an important role in degrading ubiquitinated proteins and glutamate receptors in vivo. AMSH(-/-) mice provide an animal model for neurodegenerative diseases, which are commonly characterized by the generation of proteinaceous aggregates.
    Document Type:
    Reference
    Product Catalog Number:
    AB152
    Product Catalog Name:
    Anti-Tyrosine Hydroxylase Antibody