264 research outputs found

    Culture as a Tool of Exclusion: An Analysis of Mathieu Kassovitz\u27s La Haine

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    Using the film La Haine (1995), directed by Mathieu Kassovitz, as an object of analysis, this paper explores culture as a tool of exclusion in France through sociological, architectural, and political contexts. It investigates La Haine as one of the first representations of the banlieue to mainstream French audiences, as well as the ways in which the film reveals how immigrants and children of immigrants struggle to find personal, cultural, and national identity in France

    Specific G proteins mediate endothelin induced contraction

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    Endothelin is a potent vasoconstrictor peptide which has recently been localized in the gastrointestinal tract. We have investigated the transmembrane signaling properties of endothelin in isolated smooth muscle cells of the rabbit rectosigmoid. Endothelin induced a dose dependent contraction of smooth muscle cells in a range of 10-10 to 10-6M. In normal buffer, contraction peaked at 30 sec and was sustained for up to 8 min. Incubation in 0Ca/2mM EGTA abolished the sustained contraction induced by endothelin, but had no effect on the initial transient contraction. Preincubation of saponin treated cells with G protein antisera had no effect on control cell length. Preincubation of saponin treated isolated smooth muscle cells with specific G protein antisera (rabbit antisera) for Go[alpha] or Gs for 60 minutes did not inhibit contraction induced by endothelin. Preincubation with an antiserum to Gi3[alpha] inhibited the initial transient contraction induced by endothelin and preincubation with an antiserum to Gi1-2[alpha] inhibited the sustained phase of the endothelin induced contraction. Our data indicate that: 1) Endothelin induces a direct sustained contraction of smooth cells from the rectosigmoid; 2) The transmembrane signalling of endothelin is through two specific GTP binding components that are Gi[alpha], one for the initial transient contraction, and the other for the sustained phase of the contraction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30373/1/0000775.pd

    HIF-1 and c-Src Mediate Increased Glucose Uptake Induced by Endothelin-1 and Connexin43 in Astrocytes

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    In previous work we showed that endothelin-1 (ET-1) increases the rate of glucose uptake in astrocytes, an important aspect of brain function since glucose taken up by astrocytes is used to supply the neurons with metabolic substrates. In the present work we sought to identify the signalling pathway responsible for this process in primary culture of rat astrocytes. Our results show that ET-1 promoted an increase in the transcription factor hypoxia-inducible factor-1α (HIF-1α) in astrocytes, as shown in other cell types. Furthermore, HIF-1α-siRNA experiments revealed that HIF-1α participates in the effects of ET-1 on glucose uptake and on the expression of GLUT-1, GLUT-3, type I and type II hexokinase. We previously reported that these effects of ET-1 are mediated by connexin43 (Cx43), the major gap junction protein in astrocytes. Indeed, our results show that silencing Cx43 increased HIF-1α and reduced the effect of ET-1 on HIF-1α, indicating that the effect of ET-1 on HIF-1α is mediated by Cx43. The activity of oncogenes such as c-Src can up-regulate HIF-1α. Since Cx43 interacts with c-Src, we investigated the participation of c-Src in this pathway. Interestingly, both the treatment with ET-1 and with Cx43-siRNA increased c-Src activity. In addition, when c-Src activity was inhibited neither ET-1 nor silencing Cx43 were able to up-regulate HIF-1α. In conclusion, our results suggest that ET-1 by down-regulating Cx43 activates c-Src, which in turn increases HIF-1α leading to the up-regulation of the machinery required to take up glucose in astrocytes. Cx43 expression can be reduced in response not only to ET-1 but also to various physiological and pathological stimuli. This study contributes to the identification of the signalling pathway evoked after Cx43 down-regulation that results in increased glucose uptake in astrocytes. Interestingly, this is the first evidence linking Cx43 to HIF-1, which is a master regulator of glucose metabolism

    Methylation and Eukaryotic Gene Activation

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    Lowered intraocular pressure in a glaucoma patient after intravitreal injection of ocriplasmin

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    Michael McClintock,1 Mathew W MacCumber1,2 1Department of Ophthalmology, Rush University Medical Center, 2Illinois Retina Associates, S.C., Chicago, IL, USA Abstract: We report the case of a glaucoma patient who received a single intravitreal injection of 125 µg ocriplasmin for vitreomacular traction in the right eye. The patient had bilateral advanced glaucoma and had previously undergone an implantation of an Ahmed glaucoma valve in the right eye and trabeculectomy in both eyes. The patient was using three topical ophthalmic intraocular pressure (IOP)-lowering medications on the day of injection. Baseline uncorrected Snellen visual acuity was 20/80-1 and IOP was 19 mmHg. Resolution of vitreomacular traction was achieved 1 week after injection. IOP was transiently decreased, reaching a maximum reduction of 12 mmHg below baseline at 1 month after injection, when serous choroidal effusion was also present. IOP returned to baseline levels and choroidal effusion resolved at 2 months after injection of IOP-lowering medication. Vitrectomy with epiretinal membrane and internal limiting membrane peeling, endolaser photocoagulation, and fluid–gas exchange were performed in the right eye ~3.5 months after injection to treat persistent epiretinal membrane, and presumed tractional retinal detachment. Final visual acuity was 20/50+ and IOP was 18 mmHg at 16 weeks after surgery. To our knowledge, this is the first report of IOP reduction and serous choroidal effusion after ocriplasmin injection. Keywords: ocriplasmin, intraocular pressure, vitrectomy, choroidal effusio

    INDOCYANINE GREEN ANGIOGRAPHIC FINDINGS OF HYPERTENSIVE CHOROIDOPATHY

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    Preservation of anterior capsule

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    Endothelin in brain: receptors, mitogenesis, and biosynthesis in glial cells.

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