Search Results - (Author, Cooperation:M. Saeed)

2014-06-06

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Administration, Oral ; Antiviral Agents/administration & dosage/*pharmacology/*therapeutic use ; Drug Resistance, Viral ; Hepacivirus/*drug effects ; Hepatitis C/diagnosis/*drug therapy/*virology ; Humans ; Interferon Type I/administration & dosage/pharmacology/therapeutic use ; Ribavirin/administration & dosage/pharmacology/therapeutic use ; Sofosbuvir ; Uridine Monophosphate/analogs & derivatives/pharmacology/therapeutic use

2015-08-13

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Antioxidants/metabolism ; Carcinoma, Hepatocellular/genetics/*metabolism/*virology ; Carrier Proteins/genetics/*metabolism ; *Cell Culture Techniques ; Cell Line, Tumor ; Cells, Cultured ; Gene Library ; Genome, Viral/genetics ; *Genotype ; Hepacivirus/*genetics/*growth & development/physiology ; Host-Derived Cellular Factors/genetics/*metabolism ; Humans ; Lentivirus/genetics ; Lipid Peroxidation ; Lipoproteins/genetics/*metabolism ; Mutation/genetics ; RNA, Viral/biosynthesis/genetics ; Replicon/genetics ; Serum/virology ; Trans-Activators/genetics/*metabolism ; Transduction, Genetic ; *Virus Replication/genetics ; Vitamin E/metabolism

2018-11-28

Institute of Physics (IOP)

1757-8981

1757-899X

Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics

2018-06-16

Institute of Physics (IOP)

1757-8981

1757-899X

Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Abstract: The effects of pharmacologically relevant concentrations of ethanol on the release of endogenous adenosine from rat cerebellar synaptosomes were investigated. Release was conducted for 5, 10, 30, or 60 s after which time the incubation medium (containing the released adenosine) was rapidly separated from the synaptosomal membranes by vacuum filtration. The adenosine content of the filtrate was measured by HPLC–fluorescence detection. Both basal and KCl-stimulated adenosine release consisted of an initial rapid phase, for the first 10 s, that was followed by a relatively slower phase. Basal endogenous adenosine release was estimated as 199 ± 14 pmol/mg protein/5 s. Potassium (chloride) increased adenosine release from the basal level to 433 ± 83 pmol/mg protein/5 s. Ethanol caused a dose-dependent increase of adenosine release. The interaction between dilazep and ethanol indicates that ethanol-stimulated release does not involve the dilazep-sensitive transport system. The results support previous findings that indicate that cerebellar adenosine is involved in the mediation of ethanol-induced motor disturbances in the rat.

Electronic Resource

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1749-6632

Blackwell Publishing Journal Backfiles 1879-2005

Natural Sciences in General

Electronic Resource

1365-2044

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1365-2044

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1546-1718

Nature Archives 1869 - 2009

Biology

Medicine

[Auszug] Gadd45a-null mice generated by gene targeting exhibited several of the phenotypes characteristic of p53-deficient mice, including genomic instability, increased radiation carcinogenesis and a low frequency of exencephaly. Genomic instability was exemplified by aneuploidy, chromosome ...

Electronic Resource

1365-2044

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1435-1463

Springer Online Journal Archives 1860-2000

Medicine

Summary The effect of acute ethanol on the levels of NE, DA and its metabolites DOPAC and HVA, as well as on the levels of GABA, in the corpus striatum and hypothalamus were investigated in mice in the first two hours after acute ethanol administration. There was a marked increase in the concentration of DOPAC and HVA in the corpus striatum from 30 to 120 minutes after a dose of 3.5 g/kg of ethanol even though the concentration of DA was only elevated at 60 minutes after ethanol. A dose of 1.75 g/kg of ethanol did not increase DA levels 60 minutes after administration although it did increase the concentration of DOPAC and HVA at this time. In the hypothalamus a dose of 3.5 g/kg of ethanol did not change the concentration of NE or DA but did produce a marked increase in the levels of DOPAC and HVA at 60 and 120 minutes post ethanol. A lower dose of ethanol, 1.75 g/kg, produced the same effect 60 minutes after ethanol. Ethanol caused a dose-dependent accumulation of DOPA in the corpus striatum after inhibition of DOPA-decarboxylase suggesting an increased synthesis of DA. These data suggest that the increased concentrations of DA metabolites after ethanol is secondary to enhanced DA synthesis and turnover. The concentration of NE and GABA in the hypothalamus and the corpus striatum was unchanged at any time period after ethanol.

Electronic Resource

1436-5073

Springer Online Journal Archives 1860-2000

Chemistry and Pharmacology

Zusammenfassung Zinkspuren (∼10−8 M) lassen sich mit einer benzolischen, 0,1 M Lösung von Diphenyl(2-pyridyl)methan (DPPM) aus neutralen oder sauren, wäßrigen Rhodanidlösungen durch eine einzige Extraktion ausschütteln. Jedenfalls sind 1–5 min hinreichend für die Einstellung des Gleichgewichtes. Der Einfluß der Konzentration der Mineralsäure, des Reagens, des Komplexbildners und des Aussalzmittels sowie des Volumenverhältnisses der Phasen auf die Metallextraktion wurde beschrieben. Die Extraktion erfolgt vorherrschend durch Solvatation und zwar als Zn(SCN)2(DPPM)2. Unter den gewöhnlichen Salzen beeinträchtigt nur NaCl in hoher Konzentration die Extraktion in geringem Maß. Das Metall kann aus der organischen Phase mit wäßrigen Oxalat-, Citrat- oder Acetatlösungen in einem Arbeitsgang rückextrahiert werden. Die Verteilungskoeffizienten und Trennungsfaktoren für einige Metallionen in bezug auf Zink in 0,2M Kaliumrhodanid bei optimaler Mineralsäurekonzentration wurden angegeben. Das Verfahren eignet sich für die gleichzeitige Anreicherung toxischer Metalle, wie Zn, Cu und Hg aus neutraler Lösung bei der Untersuchung der Gewässerverunreinigung.

Summary Tracer (∼10−8 M) zinc can be quantitatively extracted with 0.1M diphenyl(2-pyridyl)methane (DPPM) in benzene from neutral and acidic aqueous thiocyanate solutions in a single extraction. In all cases, extraction times of 1–5 min are sufficient for equilibration. The effects of the concentration of the mineral acids, the reagent, complexing and salting-out agents and phase-volume ratios on the metal extraction are reported. The metal is predominantly extracted through solvation, and the extraction of the metal as Zn(SCN)2(DPPM)2 is indicated. Among the common salts only sodium chloride exerts a slight depressing effect on extraction when present in high concentration. The metal can be stripped from the organic phase with aqueous oxalate, citrate or acetate solutions in a single operation. Distribution coefficients and separation factors for a number of metal ions, relative to zinc, are reported for 0.2M potassium thiocyanate media that contain the optimal concentration of mineral acid. The method can be employed for the simultaneous preconcentration of toxic metals such as zinc, copper and mercury from neutral aqueous solution in water pollution studies.

Electronic Resource

0730-2312

transfection ; CAT assays ; gene expression ; Life and Medical Sciences ; Cell & Developmental Biology

Wiley InterScience Backfile Collection 1832-2000

Biology

Chemistry and Pharmacology

Medicine

We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. The ER-negative cells inherently express lower levels of RARα and retinoic acid response element (RARE)-mediated RA-induced CAT activity. In this study we report that when ER-negative MDA-MB-231 cells were transfected with the ER gene they not only expressed higher levels of RARα and RARE-mediated RA-induced CAT gene expression, but their growth was now inhibited by RA. Estrogen enhanced RARα gene expression not only in established ER-positive cell lines but also in ER-transfected MDA-MB-231 cells. The estrogen effect appears to be direct and at the gene transcription level since it did not alter the stability of RARα mRNA and cycloheximide failed to block estrogen-mediated enhancement of RARα gene expression. Our data strongly suggest that ER-mediated enhancement of RARα levels plays an important role in RA inhibition of HBC growth. In addition, we also report here that HBC cells appear to express a unique isoform(s) of RARα which was detected only when the full-length RARα cDNA was used as a probe; the RARα1 and RARα2 specific probes failed to hybridize with the HBC specific RARα message.

8 Ill.

Electronic Resource

0730-2312

gene regulation ; stable transfection ; CAT assay ; sodium butyrate ; mRNA ; Life and Medical Sciences ; Cell & Developmental Biology

Wiley InterScience Backfile Collection 1832-2000

Biology

Chemistry and Pharmacology

Medicine

A number of studies suggest that an inverse correlation exists between the epidermal growth factor-receptor and the estrogen receptor expression in primary human breast carcinoma as well as in established human breast carcinoma cell lines. Recent studies suggest that the epidermal growth factor-receptor does not regulate the estrogen receptor gene expression. Whether the estrogen receptor regulates the epidermal growth factor-receptor gene expression is not known. We addressed this question by stably transfecting the estrogen receptor cDNA into the estrogen receptor-negative human breast carcinoma cell line MDA-MB-231. Constitutive expression of functional estrogen receptors in the transfactants resulted in increased mRNA levels of both epidermal growth factor-receptor and transforming growth factor α. Estradiol treatment of transfected cells, although enhancing transforming growth factor α mRNA levels, did not modulate epidermal growth factor-receptor mRNA levels. The estrogen receptor-transfected cells grown in estrogenic regular medium, however, exhibited lower constitutive levels of epidermal growth factor-receptor mRNA than in steroid-stripped medium, suggesting that estrogens coupled with some factors normally present in the regular medium may indeed downmodulate epidermal growth factor-receptor mRNA. Sodium butyrate treatment enhanced epidermal growth factor-receptor mRNA levels in nontransfected cells grown in regular estrogenic as well as in steroid stripped medium. Sodium butyrate enhancement of epidermal growth factor-receptor mRNA levels was completely abolished in estrogen receptor-transfected cells grown in regular estrogenic medium and blunted in steroid stripped medium. Using various epidermal growth factor-receptor gene promoter-CAT constructs in transient transfection assays, we further demonstrate that sodium butyrate enhanced transcription of the epidermal growth factor-receptor gene. The putative sodium butyrate responsive element(s) appears to localize within the proximal 384 bp of the epidermal growth factor-receptor gene promoter region. Although the interactions between estrogen receptor and epidermal growth factor-receptor are rather complex, taken together, our data suggest that estrogen receptor can indeed modulate the epidermal growth factor-receptor mRNA expression.

7 Ill.

Electronic Resource

0021-9541

Life and Medical Sciences ; Cell & Developmental Biology

Wiley InterScience Backfile Collection 1832-2000

Biology

Medicine

The insulin-like growth factors (IGFs) are potent mitogens for malignant cell proliferation. The majority of secreted IGFs are bound to specific IGF-binding proteins (IGFBPs) that are secreted by a large number of cells. These proteins may either inhibit or enhance IGF actions. Breast carcinoma cells secrete a variety of IGFBPs. We have previously demonstrated that retinoic acid (RA) inhibition of IGF-l- stimulated MCF-7 cell proliferation is associated with increased IGFBP-3 levels in the conditioned media. We therefore investigated the effect of recombinant IGFBP-3 as well as IGFBP-2, -4 and -5 on IGF-l stimulation of DNA synthesis and IGF-I binding in the MCF-7 human breast carcinoma cell line. IGFBP-2 and -3 enhanced IGF-l stimulation of DNA synthesis in MCF-7 cells while IGFBP-4 and -5 had no effect. Transfection of MCF-7 cells with an IGFBP-3 expression vector resulted in the enhanced secretion of IGFBP-3 with an accompanying increase in IGF-l binding as well as increased cell proliferation upon treatment of the cells with IGF-l. IGF-l preincubation of MCF-7 cells transfected with control pSVneo plasmids results in cells refractory to further IGF-l stimulation of thymidine incorporation while IGF-l continues to stimulate [3H]-thymidine incorporation in IGFBP-3-transfected MCF-7 cells, suggesting that IGFBP-3 protects the cells from IGF-l-mediated down regulation of its receptor. Therefore, IGFBP-3 secreted by MCF-7 cells can enhance IGF-l stimulation of DNA synthesis, increase IGF-l binding to these cells, and prevent IGF-l-induced desensitization of its own receptor, suggesting that IGFBP-3 plays a significant role in IGF-l-mediated breast carcinoma proliferation. © 1994 Wiley-Liss, Inc.

10 Ill.

Electronic Resource

0021-9541

Life and Medical Sciences ; Cell & Developmental Biology

Wiley InterScience Backfile Collection 1832-2000

Biology

Medicine

Insulin-like growth-factors I and II (IGF-I, II) are potent mitogens for breast carcinoma proliferation. In extracellular fluids, most of the IGF-I and II is associated with specific IGF-binding proteins (IGFBPs). The role of these IGFBPs in IGF action is still not clear, but it has been demonstrated that these proteins may either enhance or inhibit IGF-mediated cellular effects. Synthesis and secretion of IGFBPs have been demonstrated in breast carcinoma cells. In this study, we examined retinoic acid (RA) and IGF-I modulation of IGFBP mRNA and IGFBP levels in two ER-negative human breast carcinoma cell lines. Treatment of MDAMB-231 and MDA-MB-468 cells with RA increased the levels in conditioned media of a Mr 42-46-kDa IGFBP, which was immunoprecipitated by an IGFBP-3 antibody. IGF-I also increased the accumulated levels of IGFBP-3 in the conditioned media of both cell lines. Both cell lines expressed high basal levels of IGFBP-3 mRNA; the addition of RA increased IGFBP-3 mRNA levels by 1.5-fold, whereas the addition of IGFI had no effect on IGFBP-3 mRNA levels in either cell line. The difference in the magnitude of the RA enhancement of IGFBP-3 mRNA levels (1.5-fold) and RA stimulation of IGFBP-3 levels in conditioned media (3.5-4-fold) suggests that some of the effect of RA is at a posttranscriptional level. IGF-I increased the levels of IGFBP-2 and IGFBP-5 in conditioned media by greater than tenfold but had no effect on IGFBP-2 and IGFBP-5 mRNA levels, again suggesting the involvement of posttranscriptional controls. Pretreatment of MDA-MB-468 and MDA-MB-231 cells with IGF-I receptor antibody (αIR3) blocked the IGF-I effect on IGFBP-3 levels in the media in both cell lines and IGFBP-2 and IGFBP-5 secreted levels in MDA-MB-468 cell conditioned media. The addition of RA also blocked IGF-I stimulation of IGFBP2 and IGFBP-5 levels. Cycloheximide treatment completely blocked the RA and/or IGF-I-mediated modulation of these binding proteins, suggesting that these agents enhance IGFBP-3, IGFBP-2, and IGFBP-5 synthesis and consequent secretion. MDA-MB-468 cells expressed IGFBP-5 mRNA, whereas both MDA-MB-231 and MDA-MB-468 expressed IGFBP-6 mRNA. RA enhanced IGFBP-6 gene expression by threefold in MDA-MB-231 cells, whereas IGF-1 had no effect on IGFBP-6 gene expression in either cell line. These results demonstrate that RA and IGF-I modulate IGFBP levels in a number of breast carcinoma cell lines. Such modulation of IGFBPs may in turn affect IGF mediated cellular responses and thus the biologic behavior of these malignant cells.

10 Ill.

Electronic Resource

0021-9541

Life and Medical Sciences ; Cell & Developmental Biology

Wiley InterScience Backfile Collection 1832-2000

Biology

Medicine

Retinoids modulate cellular proliferation and mediate gene function through a series of nuclear receptors. The retinoic acid nuclear receptor β (RARβ) plays an important role in the differentiation of a number of cell types. We now demonstrate that RARβ expresion is confined to normal mammary tissue and is not expressed in either immortalized normal or malignant cell lines. Treatment of RARβ-transfected MDA-MB-231 cells with 1 μM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RARβ. RARβ-expressing MDA-MB-231 cells formed significantly smaller and fewer colonies soft agar than the mock-transfected cells. Addition of 1 μM RA stimulated colony size and number in the RARβ-transfected MDA-MB-231 cells. In contast to the RARβ-expressing cells, colony formation by the RARβ-expressing cells was similar to the mock-transfected controls and the addition of 1 μM RA to the RARα-transfected cells inhibited colony formation. While demonstrating decreased colony formation in agar, RARβ-expressing MDA-MB-231 cells failed to exhibit decreased growth in SCID mice. Our results show that RARβ functions as a negative regulator of growth in breast epithelial cells. In addition, the growth of these cells is differentially regulated by RARα and RARβ which is most likely the result to the modulation of different genes. © 1995 Wiley-Liss Inc.

6 Ill.

Electronic Resource

2018-08-14

American Physical Society (APS)

1098-0121

1095-3795

Physics

Semiconductors II: surfaces, interfaces, microstructures, and related topics

2018-09-18

The American Association of Immunologists (AAI)

0022-1767

1550-6606

Medicine