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  • Nicotine-Induced Structural Plasticity in Mesencephalic Dopaminergic Neurons Is Mediated by Dopamine D3 Receptors and Akt-mTORC1 Signaling. 23543412

    Although long-term exposure to nicotine is highly addictive, one beneficial consequence of chronic tobacco use is a reduced risk for Parkinson's disease. Of interest, these effects both reflect structural and functional plasticity of brain circuits controlling reward and motor behavior and, specifically, recruitment of nicotinic acetylcholine receptors (nAChR) in mesencephalic dopaminergic neurons. Because the underlying cellular mechanisms are poorly understood, we addressed this issue with use of primary cultures of mouse mesencephalic dopaminergic neurons. Exposure to nicotine (1-10 μM) for 72 hours in vitro increased dendritic arborization and soma size in primary cultures. These effects were blocked by mecamylamine and dihydro-β-erythroidine, but not methyllycaconitine. The involvement of α4β2 nAChR was supported by the lack of nicotine-induced structural remodeling in neurons from α4 null mutant mice (KO). Challenge with nicotine triggered phosphorylation of the extracellular signal-regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mammalian target of rapamycin complex 1 (mTORC1)-dependent p70 ribosomal S6 protein kinase. Upstream pathway blockade using the phosphatidylinositol 3-kinase inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one hydrochloride] resulted in suppression of nicotine-induced phosphorylations and structural plasticity. These effects were dependent on functional DA D3 receptor (D3R), because nicotine was inactive both in cultures from D3R KO mice and after pharmacologic blockade with D3R antagonist trans-N-4-2-(6-cyano-1,2,3, 4-tetrahydroisoquinolin-2-yl)ethylcyclohexyl-4-quinolinecarboxamide (SB-277011-A) (50 nM). Finally, exposure to nicotine in utero (5 mg/kg/day for 5 days) resulted in increased soma area of DAergic neurons of newborn mice, effects not observed in D3 receptor null mutant mice mice. These findings indicate that nicotine-induced structural plasticity at mesencephalic dopaminergic neurons involves α4β2 nAChRs together with dopamine D3R-mediated recruitment of ERK/Akt-mTORC1 signaling.
    Document Type:
    Reference
    Product Catalog Number:
    AB152
    Product Catalog Name:
    Anti-Tyrosine Hydroxylase Antibody

  • Patterns of illness in the highly febrile young child: epidemiologic, clinical, and laboratory correlates. 6973132

    Three hundred one episodes of fever greater than or equal to 103 F were documented in 375 infants and young children observed in a comprehensive care clinic during the period October 1974 to October 1978. Of such highly febrile illnesses 79% were accompanied by respiratory tract signs or symptoms, 7% by disease at a site other than the respiratory tract, and 22% of illnesses had no localizing signs or symptoms. Viral cultures were obtained from the respiratory tract in 178 cases and were positive in 68: 57/134 from respiratory illness; 2/4 from illness at sites other than the respiratory tract; and 9/40 in children without localizing disease. Bacterial cultures of the upper respiratory tract were obtained in 191 illnesses, but the overall rate of isolation of Haemophilus influenzae, Streptococcus pneumoniae and group A streptococci (46%) did not differ from that in a group of well children (39%). Bacterial cultures of the blood were obtained in 89 patients with fever greater than or equal to 103 F and in an additional 41 children with lower temperatures. Nine children had documented systemic bacterial disease (eight positive blood cultures and one positive CSF). The rate of clinically apparent systemic bacterial disease in these otherwise normal infants was one bacteremic episode per 94 years of child care.
    Document Type:
    Reference
    Product Catalog Number:
    3296

  • Plasma vitamin C is inversely related to body mass index and waist circumference but not to plasma adiponectin in nonsmoking adults. 17585027

    We examined the relationships between plasma vitamin C, adiposity, and the collagen-like adipokine, adiponectin. Of 118 sedentary, nonsmoking adults participating in the cross-sectional trial (35 men and 83 women aged 38.7 +/- 1.0 y with BMI of 30.4 +/- 0.6 kg/m2, plasma vitamin C concentrations of 43.5 +/- 1.3 micromol/L, and plasma adiponectin concentrations of 8.9 +/- 0.3 mg/L), 54% were obese and 24% were overweight. Plasma vitamin C was inversely related to BMI, percentage of body fat, and waist circumference in both women and men (r = -0.383 to -0.497, P 0.025). In women but not men, these associations remained significant after controlling for body mass. Plasma vitamin C was directly related to plasma adiponectin in the women after controlling for age and vitamin C supplement use (r = 0.222, P = 0.049) but not after controlling for body mass. Twenty obese men and women participated in an intervention trial and consumed an energy-restricted diet low in vitamin C (approximately 38 mg/d) for 8 wk. Subjects were stratified by age, gender, and BMI and randomly assigned to receive placebo or vitamin C (500 mg) capsules daily. At baseline, plasma adiponectin was directly related to plasma vitamin C (r = 0.609, P = 0.021) and inversely related to body mass (r = -0.785, P = 0.001). Body mass decreased significantly during the 8 wk study in both the vitamin C (n = 6, -5.9 +/- 0.9 kg) and placebo groups (n = 8, -6.5 +/- 0.7 kg). Plasma adiponectin increased 13% from baseline by wk 8 in both groups (P 0.05). In summary, plasma vitamin C was inversely related to markers of adiposity, particularly in women, but vitamin C supplementation did not influence the circulating concentration of adiponectin.
    Document Type:
    Reference
    Product Catalog Number:
    HADP-61HK
    Product Catalog Name:
    Human Adiponectin RIA

  • Recipients of vaccine against the 1976 "swine flu" have enhanced neutralization responses to the 2009 novel H1N1 influenza virus. 20415539

    BACKGROUND. The world is facing a novel H1N1 influenza pandemic. A pandemic scare with a similar influenza virus in 1976 resulted in the vaccination of nearly 45 million persons. We hypothesized that prior receipt of the 1976 "swine flu" vaccine would enhance immune responses to the 2009 novel H1N1 influenza strain. METHODS. A prospective, volunteer sample of employees aged greater than or = 55 years at a children's cancer hospital in August 2009 was assessed for antibody responses to the 2009 pandemic H1N1 influenza virus and the 2008-2009 seasonal H1N1 influenza virus. RESULTS. Antibody responses by hemagglutination-inhibition assay were high against both the seasonal influenza virus (89.7% had a titer considered seroprotective) and pandemic H1N1 influenza virus (88.8% had a seroprotective titer). These antibodies were effective at neutralizing the seasonal H1N1 influenza virus in 68.1% of participants (titer greater than or = 40), but only 18.1% had detectable neutralizing titers against the pandemic H1N1 influenza virus. Of 116 participants, 46 (39.7%) received the 1976 "swine flu" vaccine. Receipt of this vaccine significantly enhanced neutralization responses; 8 (17.4%) of 46 vaccine recipients had titers greater than or = 160, compared with only 3 (4.3%) of 70 who did not receive the vaccine (P = .018 by chi(2) test). CONCLUSIONS. In this cohort, persons aged greater than or = 55 years had evidence of robust immunity to the 2008-2009 seasonal H1N1 influenza virus. These antibodies were cross-reactive but nonneutralizing against the 2009 pandemic H1N1 influenza strain. Receipt of a vaccine to a related virus significantly enhanced the neutralization capacity of these responses, suggesting homologous vaccination against the 2009 pandemic H1N1 influenza virus would have a similar effect.
    Document Type:
    Reference
    Product Catalog Number:
    MAB8251
    Product Catalog Name:
    Anti-Influenza A Antibody, nucleoprotein, clones A1, A3 Blend

  • Phospholipid scramblase 1 binds to the promoter region of the inositol 1,4,5-triphosphate receptor type 1 gene to enhance its expression. 16091359

    Phospholipid scramblase 1 (PLSCR1) is a multiply palmitoylated, endofacial membrane protein originally identified based on its capacity to promote accelerated transbilayer phospholipid movement in response to Ca(2+). Recent evidence suggests that this protein also participates in cell response to various growth factors and cytokines, influencing myeloid differentiation, tumor growth, and the antiviral activity of interferon. Whereas plasma membrane PLSCR1 was shown to be required for normal recruitment and activation of Src kinase by stimulated cell surface growth factor receptors, PLSCR1 was also found to traffic into the nucleus and to tightly bind to genomic DNA, suggesting a possible additional nuclear function. We now report evidence that PLSCR1 directly binds to the 5'-promoter region of the inositol 1,4,5-triphosphate receptor type 1 gene (IP3R1) to enhance expression of the receptor. Probing a CpG island genomic library with PLSCR1 as bait identified four clones with avidity for PLSCR1, including a 191-bp fragment of the IP3R1 promoter. Using electrophoretic mobility shift and transcription reporter assays, the PLSCR1-binding site in IP3R1 was mapped to residues (-101)GTAACCATGTGGA(-89), and the segment spanning Met(86)-Glu(118) in PLSCR1 was identified to mediate its transcriptional activity. The significance of this interaction between PLSCR1 and IP3R1 in situ was confirmed by comparing levels of IP3R1 mRNA and protein in matched cells that either expressed or were deficient in PLSCR1. These data suggest that in addition to its role at the plasma membrane, effects of PLSCR1 on cell proliferative and maturational responses may also relate to alterations in expression of cellular IP3 receptors.
    Document Type:
    Reference
    Product Catalog Number:
    MABS483
    Product Catalog Name:
    Anti-PL Scramblase 1 Antibody, clone 4D2

  • The relationship between ovarian progesterone and proteolytic enzyme activity during ovulation in the gonadotropin-treated immature rat. 1536908

    To clarify the mechanisms by which progesterone acts as a mediator in the ovulatory process, ovulation rate and proteolytic enzyme activities were investigated in immature 22-day-old rats treated with PMSG/hCG, RU486 (10 mg/kg), synthetic antiprogesterone, and RU486 (10 mg/kg) + progesterone (10 mg/kg). The number of ova was significantly decreased when RU486 (10 mg/kg) was given from 2 h before to 4 h after the hCG injection. In addition, its inhibitory action on ovulation was reversed by exogenous progesterone (10 mg/kg) at 2 or 4 h after the hCG injection. Serum progesterone and estradiol concentrations in the rats treated with RU486 did not show any significant differences compared to controls. The proteolytic enzyme activities were measured by using the synthetic substrates alpha-N-benzoyl-DL-Arg-beta naphthylamide (BANA) and dinitrophenyl peptide (DNP). Activities were significantly increased after hCG injection in the control group during 8-9 h for BANA hydrolase and 7-10 h for DNP peptidase. The preovulatory increase of these activities was totally suppressed by RU486 with hCG. After administration of progesterone (10 mg/kg) following hCG and RU486 injection, the elevation of proteolytic, enzyme activities in the preovulatory phase was effectively reversed, and levels became similar to those in the control group. These results suggest that progesterone plays an indispensable role in the first 4 h of the ovulatory process by regulating proteolytic enzyme activities.
    Document Type:
    Reference
    Product Catalog Number:
    20-176
    Product Catalog Name:
    100X GTPγS, 10mM

  • Erythrocyte-bound apolipoprotein B in relation to atherosclerosis, serum lipids and ABO blood group. 24069429

    Erythrocytes carry apolipoprotein B on their membrane, but the determining factors of erythrocyte-bound apolipoprotein B (ery-apoB) are unknown. We aimed to explore the determinants of ery-apoB to gain more insight into potential mechanisms.Subjects with and without CVD were included (N = 398). Ery-apoB was measured on fresh whole blood samples using flow cytometry. Subjects with ery-apoB levels ≤ 0.20 a.u. were considered deficient. Carotid intima media thickness (CIMT) was determined as a measure of (subclinical) atherosclerosis.Mean ery-apoB value was 23.2% lower in subjects with increased CIMT (0.80 ± 0.09 mm, N = 140) compared to subjects with a normal CIMT (0.57 ± 0.08 mm, N = 258) (P = 0.007, adjusted P<0.001). CIMT and ery-apoB were inversely correlated (Spearman's r: -0.116, P = 0.021). A total of 55 subjects (13.6%) were considered ery-apoB deficient, which was associated with a medical history of CVD (OR: 1.86, 95% CI 1.04-3.33; adjusted OR: 1.55; 95% CI 0.85-2.82). Discontinuation of statins in 54 subjects did not influence ery-apoB values despite a 58.4% increase in serum apolipoprotein B. Subjects with blood group O had significantly higher ery-apoB values (1.56 ± 0.94 a.u.) when compared to subjects with blood group A (0.89 ± 1.15 a.u), blood group B (0.73 ± 0.1.12 a.u.) or blood group AB (0.69 ± 0.69 a.u.) (P-ANOVA = 0.002).Absence or very low values of ery-apoB are associated with clinical and subclinical atherosclerosis. While serum apolipoprotein B is not associated with ery-apoB, the ABO blood group seems to be a significant determinant.
    Document Type:
    Reference
    Product Catalog Number:
    AB742
    Product Catalog Name:
    Anti-Apolipoprotein B Antibody

  • Certificate of Analysis 178494_D00087617

    Document Type:
    Certificate of Analysis
    Lot Number:
    D00087617
    Product Catalog Number:
    178494
    Product Catalog Name:
    Apoptosis Inhibitor II, NS3694 - CAS 426834-38-0 - Calbiochem

  • Certificate of Analysis 178494_3147649

    Document Type:
    Certificate of Analysis
    Lot Number:
    3147649
    Product Catalog Number:
    178494
    Product Catalog Name:
    Apoptosis Inhibitor II, NS3694 - CAS 426834-38-0 - Calbiochem