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Wards of the State: regnant and prostitute women Wards of the State: regnant and prostitute women
Gail Pheterson
Política y Sociedad , 2009, DOI: -
Abstract: The paper demonstrates common mechanisms underlying state control of prostitute and pregnant women. On a global level, institutional regulation of pregnancy and prostitution has been incorporated into “population control” and “migration control” under the name of “family planning” and “anti trafficking”. Although those policies fit within a coherent system, reproductive and sexual issues are most often isolated, or framed as ideological and strategic opposites, also by feminist theorists and activists. This false dichotomy reinforces the division of women and colludes with social hypocrisy and injustice. El artículo muestra los mecanismos comunes subyacentes en el control estatal a mujeres prostitutas y embarazadas. Aun nivel global, la regulación institucional del embarazo y de la prostitución ha sido incorporada al “control de la población” y al “control de la migración” bajo el nombre de “planeamiento familiar” y “antitráfico”. Aunque estas políticas se incluyen dentro de un sistema coherente, las cuestiones sobre reproducción y sexualidad son muy a menudo aisladas o enmarcadas como oposiciones ideológicas y estratégicas, incluso por feministas teóricos y activistas. Esta falsa dicotomía refuerza la división de la mujer y refuerza la hipocresía social y la injusticia.
Growth-Arrest-Specific Protein 2 Inhibits Cell Division in Xenopus Embryos  [PDF]
Tong Zhang, Bama Dayanandan, Isabelle Rouiller, Elizabeth J. Lawrence, Craig A. Mandato
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0024698
Abstract: Background Growth-arrest-specific 2 gene was originally identified in murine fibroblasts under growth arrest conditions. Furthermore, serum stimulation of quiescent, non-dividing cells leads to the down-regulation of gas2 and results in re-entry into the cell cycle. Cytoskeleton rearrangements are critical for cell cycle progression and cell division and the Gas2 protein has been shown to co-localize with actin and microtubules in interphase mammalian cells. Despite these findings, direct evidence supporting a role for Gas2 in the mechanism of cell division has not been reported. Methodology and Principal Findings To determine whether the Gas2 protein plays a role in cell division, we over-expressed the full-length Gas2 protein and Gas2 truncations containing either the actin-binding CH domain or the tubulin-binding Gas2 domain in Xenopus laevis embryos. We found that both the full-length Gas2 protein and the Gas2 domain, but not the CH domain, inhibited cell division and resulted in multinucleated cells. The observation that Gas2 domain alone can arrest cell division suggests that Gas2 function is mediated by microtubule binding. Gas2 co-localized with microtubules at the cell cortex of Gas2-injected Xenopus embryos using cryo-confocal microscopy and co-sedimented with microtubules in cytoskeleton co-sedimentation assays. To investigate the mechanism of Gas2-induced cell division arrest, we showed, using a wound-induced contractile array assay, that Gas2 stabilized microtubules. Finally, electron microscopy studies demonstrated that Gas2 bundled microtubules into higher-order structures. Conclusion and Significance Our experiments show that Gas2 inhibits cell division in Xenopus embryos. We propose that Gas2 function is mediated by binding and bundling microtubules, leading to cell division arrest.
Growth Arrest of BCR-ABL Positive Cells with a Sequence-Specific Polyamide-Chlorambucil Conjugate  [PDF]
C. James Chou, Thomas O'Hare, Sophie Lefebvre, David Alvarez, Jeffrey W. Tyner, Christopher A. Eide, Brian J. Druker, Joel M. Gottesfeld
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003593
Abstract: Chronic myeloid leukemia (CML) is characterized by the presence of a constitutively active Abl kinase, which is the product of a chimeric BCR-ABL gene, caused by the genetic translocation known as the Philadelphia chromosome. Imatinib, a selective inhibitor of the Bcr-Abl tyrosine kinase, has significantly improved the clinical outcome of patients with CML. However, subsets of patients lose their response to treatment through the emergence of imatinib-resistant cells, and imatinib treatment is less durable for patients with late stage CML. Although alternative Bcr-Abl tyrosine kinase inhibitors have been developed to overcome drug resistance, a cocktail therapy of different kinase inhibitors and additional chemotherapeutics may be needed for complete remission of CML in some cases. Chlorambucil has been used for treatment of B cell chronic lymphocytic leukemia, non-Hodgkin's and Hodgkin's disease. Here we report that a DNA sequence-specific pyrrole-imidazole polyamide-chlorambucil conjugate, 1R-Chl, causes growth arrest of cells harboring both unmutated BCR-ABL and three imatinib resistant strains. 1R-Chl also displays selective toxicities against activated lymphocytes and a high dose tolerance in a murine model.
Growth arrest-specific protein 6 (GAS6) and the protein C pathway
Shi-Sheng Li
Critical Care , 2007, DOI: 10.1186/cc5734
Abstract: Two recent studies revealed that the level of plasma GAS6 was elevated and was correlated with disease severity in patients with severe sepsis [4] and septic shock [5]. However, significantly different levels of plasma GAS6 between the two studies (56 to 139 ng/ml [4] and 1.5 to 164 pg/ml [5]) were reported on the basis of a similar enzyme-linked immunosorbent assay. The lack of a control group of healthy subjects in the report by Gibot and coworkers [5] prevents a direct comparison of both studies. In addition, it would be interesting to analyze the correlation between GAS6 concentrations and the outcome of APC treatment of those patients because a possible interaction between the Gla domains of GAS6 and APC might modulate the PC anticoagulant and signaling pathways.APC = activated protein C; GAS6 = growth arrest-specific protein 6; Gla = γ-carboxyglutamic acid; PAR-1 = protease-activated receptor-1; PC = protein C; PS = protein S; TSR = thrombin-sensitive region.The authors declare that they have no competing interests.
Epigenetic Transcriptional Regulation of the Growth Arrest-Specific gene 1 (Gas1) in Hepatic Cell Proliferation at Mononucleosomal Resolution  [PDF]
Natalia Sacilotto,Antonio Espert,Josefa Castillo,Luis Franco,Gerardo López-Rodas
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0023318
Abstract: Gas1 (growth arrest-specific 1) gene is known to inhibit cell proliferation in a variety of models, but its possible implication in regulating quiescence in adult tissues has not been examined to date. The knowledge of how Gas1 is regulated in quiescence may contribute to understand the deregulation occurring in neoplastic diseases.
Serial measurement of neuron specific enolase improves prognostication in cardiac arrest patients treated with hypothermia: A prospective study
Christian Storm, Jens Nee, Achim J?rres, Christoph Leithner, Dietrich Hasper, Christoph J Ploner
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2012, DOI: 10.1186/1757-7241-20-6
Abstract: In a prospective study of 35 patients resuscitated from cardiac arrest, NSE was measured daily for four days following admission. Outcome was assessed at ICU discharge using the CPC score. All patients received hypothermia treatment for 24 hours at 33°C with a surface cooling device according to current guidelines.The cutoff for absolute NSE levels in patients with unfavourable outcome (CPC 3-5) 72 hours after cardiac arrest was 57 μg/l with an area under the curve (AUC) of 0.82 (sensitivity 47%, specificity 100%). The cutoff level for NSE kinetics in patients with unfavourable outcome (CPC 3-5) was an absolute increase of 7.9 μg/l (AUC 0.78, sensitivity 63%, specificity 100%) and a relative increase of 33.1% (AUC 0.803, sensitivity 67%, specificity 100%) at 48 hours compared to admission.In cardiac arrest patients treated with hypothermia, prognostication of unfavourable outcome by NSE kinetics between admission and 48 hours after resuscitation may be superior to prognostication by absolute NSE levels.The recommended examinations proposed by the American Academy of Neurology (AAN) for prognostication in patients after cardiac arrest have mainly been evaluated in the era prior to hypothermia [1]. However, recent studies indicate that mild therapeutic hypothermia modifies the prognostic significance of clinical findings, NSE levels, and electrophysiological testing in patients resuscitated from cardiac arrest [2-6]. This has generated the necessity to re-evaluate all prognostic markers in patients treated with hypothermia. In particular, NSE cutoff levels and their temporal dynamics have only rarely been investigated in these patients so far. In this study, we prospectively investigated serum NSE levels and NSE kinetics in 35 cardiac arrest patients treated with hypothermia.The study protocol was approved by the local ethics committee on human research and was conducted in accordance with the guidelines of the Declaration of Helsinki. Written informed consent to the
Growth arrest-specific protein 6 plasma concentrations during septic shock
Sébastien Gibot, Frédéric Massin, Aurélie Cravoisy, Rachel Dupays, Damien Barraud, Lionel Nace, Pierre-Edouard Bollaert
Critical Care , 2007, DOI: 10.1186/cc5158
Abstract: Forty-five patients with septic shock admitted to a medical adult intensive care unit were enrolled. Plasma Gas6 concentration was determined using enzyme-linked immunosorbent assay at days 1, 3, 7 and 14.The median (interquartile range) Gas6 concentration was 51 (5 to 95) pg/ml at admission. A positive correlation (Spearman rank-order coefficient [rs] = 0.37, P = 0.01) was found between Gas6 level and Sepsis-related Organ Failure Assessment score. Patients requiring renal support had higher Gas6 concentration that those without need for haemofiltration (76.5 [52 to 164] pg/ml versus 10.5 [1.5 to 80.5] pg/ml; P = 0.04). Moreover, there was a positive correlation between Gas6 and aspartate transaminase (rs = 0.42, P = 0.006) and between Gas6 and prothrombin time (rs = 0.45, P = 0.02). Although there was a progressive decline in Gas6 concentration in survivors (analysis of variance, P = 0.01), nonsurvivors exhibited persistently elevated Gas6. However, the two populations diverged only after day 7 (P = 0.04).Plasma concentrations of Gas6 correlate with disease severity, especially with renal and hepatic dysfunction, in septic shock.As new therapeutic options emerge for the management of septic shock, accurate prognostic factors are needed to better identify those patients who are likely to benefit. Although a number of severity scores (including Acute Physiology and Chronic Health Evaluation II score and Simplified Acute Physiology Score [SAPS]II or SAPSIII) and biological markers (procalcitonin [PCT] and C-reactive protein, among others) are available to predict outcome in critically ill patients, the appropriateness of their use during septic shock remains debatable.The product of growth arrest-specific gene 6 (Gas6) recently attracted attention because it was found to be elevated during sepsis and may correlate with organ dysfunction [1]. This vitamin K dependent protein is secreted by leucocytes and endothelial cells in response to serum starvation or injury, and
Interaction of influenza virus NS1 protein with growth arrest-specific protein 8
Lixia Zhao, Long Xu, Xiaowei Zhou, Qingyu Zhu, Zhixin Yang, Chuanfu Zhang, Xudong Zhu, Mengbin Yu, Yingying Zhang, Xinghui Zhao, Peitang Huang
Virology Journal , 2009, DOI: 10.1186/1743-422x-6-218
Abstract: Influenza A viral NS1 protein is a multifunctional protein that is capable of both protein-protein and protein-RNA interactions [1]. It binds non-specifically to double-stranded RNA and specifically to protein targets. NS1 binds directly to p85β to activate phosphatidylinositol 3-kinase signaling [2]. It binds a cleavage and polyadenylation specificity factor to inhibit the maturation and export of host antiviral mRNAs, and it inhibits poly(A)-binding protein II [3]. NS1 protein interacts with the viral RNA polymerase complex [4], the eukaryotic translation initiation factor eIF4GI [5], NS1-I [6], NS1-BP [7], Staufen [8], and nucleolin [9]. Association of NS1 protein with host factors may affect apoptosis [10,11].Growth arrest-specific genes are expressed preferentially in cultured cells that have entered a quiescent state following serum deprivation or growth to confluence. To date, eleven GAS genes have been identified that act in a variety of biological functions, including the control of microfilament organization [12], nerve cell growth or differentiation [13], apoptosis [14], tyrosine kinase receptor activity [15], and negative and positive control of the cell cycle [16,17]. No sequence similarity or common structural features have been found among the GAS genes or proteins [18].GAS8, also known as GAS11, is located at 16q24.3 and was found to be a common deletion present in breast and prostate carcinomas. It was viewed as a potential tumor suppressor gene. The GAS8 gene consists of 11 exons spanning approximately 25 kb. Northern blot analysis identified two ubiquitously expressed mRNAs of 3.4 and 1.8 kb in length. Another gene, C16orf3, lies within intron 2 of GAS8, and is transcribed in the opposite orientation of GAS8 [19].Gas8 protein associates with microtubules in vitro and in vivo. Deletion analysis identified a microtubule-binding domain (GMAD) and a region that attenuates Gas8-microtubule interactions (IMAD) [20]. Gas8 homologs in Trypanosoma brucei a
Growth Arrest Specific 2 Is Up-Regulated in Chronic Myeloid Leukemia Cells and Required for Their Growth  [PDF]
Haixia Zhou, Yue Ge, Lili Sun, Wenjuan Ma, Jie Wu, Xiuyan Zhang, Xiaohui Hu, Connie J. Eaves, Depei Wu, Yun Zhao
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086195
Abstract: Although the generation of BCR-ABL is the molecular hallmark of chronic myeloid leukemia (CML), the comprehensive molecular mechanisms of the disease remain unclear yet. Growth arrest specific 2 (GAS2) regulates multiple cellular functions including cell cycle, apoptosis and calpain activities. In the present study, we found GAS2 was up-regulated in CML cells including CD34+ progenitor cells compared to their normal counterparts. We utilized RNAi and the expression of dominant negative form of GAS2 (GAS2DN) to target GAS2, which resulted in calpain activity enhancement and growth inhibition of both K562 and MEG-01 cells. Targeting GAS2 also sensitized K562 cells to Imatinib mesylate (IM). GAS2DN suppressed the tumorigenic ability of MEG-01 cells and impaired the tumour growth as well. Moreover, the CD34+ cells from CML patients and healthy donors were transduced with control and GAS2DN lentiviral vectors, and the CD34+ transduced (YFP+) progeny cells (CD34+YFP+) were plated for colony-forming cell (CFC) assay. The results showed that GAS2DN inhibited the CFC production of CML cells by 57±3% (n = 3), while affected those of normal hematopoietic cells by 31±1% (n = 2). Next, we found the inhibition of CML cells by GAS2DN was dependent on calpain activity but not the degradation of beta-catenin. Lastly, we generated microarray data to identify the differentially expressed genes upon GAS2DN and validated that the expression of HNRPDL, PTK7 and UCHL5 was suppressed by GAS2DN. These 3 genes were up-regulated in CML cells compared to normal control cells and the growth of K562 cells was inhibited upon HNRPDL silence. Taken together, we have demonstrated that GAS2 is up-regulated in CML cells and the inhibition of GAS2 impairs the growth of CML cells, which indicates GAS2 is a novel regulator of CML cells and a potential therapeutic target of this disease.
Serum neuron-specific enolase as early predictor of outcome after in-hospital cardiac arrest: a cohort study
Tatiana H Rech, Silvia Vieira, Fabiano Nagel, Janete Brauner, Rosana Scalco
Critical Care , 2006, DOI: 10.1186/cc5046
Abstract: Forty-five patients resuscitated from in-hospital cardiac arrest were prospectively studied from June 2003 to January 2005. Blood samples were collected, at any time between 12 and 36 hours after the arrest, for NSE measurement. Outcome was evaluated 6 months later with the Glasgow outcome scale (GOS). Patients were divided into two groups: group 1 (unfavorable outcome) included GOS 1 and 2 patients; group 2 (favorable outcome) included GOS 3, 4 and 5 patients. The Mann–Whitney U test, Student's t test and Fisher's exact test were used to compare the groups.The Glasgow coma scale scores were 6.1 ± 3 in group 1 and 12.1 ± 3 in group 2 (means ± SD; p < 0.001). The mean time to NSE sampling was 20.2 ± 8.3 hours in group 1 and 28.4 ± 8.7 hours in group 2 (p = 0.013). Two patients were excluded from the analysis because of sample hemolysis. At 6 months, favorable outcome was observed in nine patients (19.6%). Thirty patients (69.8%) died and four (9.3%) remained in a persistent vegetative state. The 34 patients (81.4%) in group 1 had significantly higher NSE levels (median 44.24 ng/ml, range 8.1 to 370) than those in group 2 (25.26 ng/ml, range 9.28 to 55.41; p = 0.034).Early determination of serum NSE levels is a valuable ancillary method for assessing outcome after in-hospital cardiac arrest.Since the introduction of closed-chest cardiac massage in 1960 [1] there have been several advances in cardiopulmonary resuscitation [2]. In spite of that, morbidity and mortality associated with cardiac arrest remain extremely high [3,4], with prognosis ranging from mild to moderate disability to persistent vegetative state. It is estimated that 80% of sudden death survivors remain in a coma for various lengths of time, and a full neurological recovery is still rare [5]. The possibility of irreversible anoxic brain damage must be taken into account soon after the arrest.In this scenario, an accurate prognostic evaluation of cardiac arrest patients may have major ethical and econom
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