“Pulling the world in and pushing it away”: Participating bodies and the concept of coping

In her lead article in this special issue, Monica Greco offers the concept of participating bodies as a “possibility of conceiving bodies themselves – and bodily events such as disease/illness - as expressing values and perhaps even socially meaningful ‘preferences’.” Such a position seeks to avoid capitulation to a) an image of bodily processes as without values or responsiveness, object rather than participant; b) an image of human agents as unitary, self-knowing, sovereign choosers - unless ill. This article will explore this perspective as applied to the idea of coping. The article will explore strategies of everyday living, through particular consideration of Lauren Berlant’s reading of Two Girls, Fat and Thin by Mary Gaitskill. In her interpretation of the novel, Berlant assesses the kinds of problems for subjects and bodies that may be solved or managed through participation in or refraining from participation in thinking, food or sex. The account of coping and embodiment in Berlant’s reflections will then be placed in dialogue with findings by Alexandra Michel, who watched the process of physical burnout in investment banking associates during a thirteen-year cultural ethnography, observing as the bankers heeded or ignored the cues their bodies gave about the limits of feasible demands. The article as a whole offers an illustration of the value of Greco’s reflections for offering a fresh and valuable perspective on the concept of coping.Wellcome Trust - via grant to Goldsmiths University. Contact person at Goldsmiths is: [email protected]

Redox-sensitive small GTPase H-Ras in murine astrocytes, an in vitro study

Although the protooncogenes small GTPases Ras are redox-sensitive proteins, how they are regulated by redox signaling in the central nervous system (CNS) is still poorly understood. Alteration in redox-sensitive targets by redox signaling may have myriad effects on Ras stability, activity and localization. Redox-mediated changes in astrocytic RAS may contribute to the control of redox homeostasis in the CNS that is connected to the pathogenesis of many diseases

Fathers' attachment representations and infant feeding practices.

This study examined how fathers' adult attachment representations, assessed before the birth of their first child, predict feeding practices with their 8-month-old infants. Fathers have been underrepresented in child feeding research, particularly in longitudinal and observational studies. Feeding is a key parenting task of infancy and a growing number of studies have begun to explore the connection between attachment and parental feeding practices and behavior, revealing a clear link between mothers' adult attachment and how they feed their children. This is the first longitudinal examination of attachment as a prenatal predictor of fathers' infant feeding behavior. Participants were 118 first-time fathers and their infants. Adult Attachment Interviews were conducted in the third trimester of pregnancy, and father-infant feeding interactions were observed at home when the infant was 8-months-old. Videotaped feedings were coded using Chatoor's Feeding Scale (1997). Compared to other fathers, (1) those with secure attachment representations were more attuned to their infants during feeding, (2) those with dismissing representations were less attuned, and (3) those with unresolved trauma displayed more controlling behaviors. Fathers were more controlling with their sons than their daughters across all attachment representations. Study results suggest that father's infant feeding behaviors may influence by their own attachment representations. The links to fathers' controlling feeding practices are noteworthy because of the negative implications controlling parental feeding practices can have on child outcomes. The prediction of paternal feeding behaviors from assessments conducted prenatally has important intervention implications

Lysine-Specific Demethylase 1A as a Promising Target in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is a heterogeneous hematopoietic malignancy characterized by the accumulation of incompletely differentiated progenitor cells (blasts) in the bone marrow and blood, and by suppression of normal hematopoiesis. It has recently become apparent that the AML genome is characterized by recurrent mutations and dysregulations in epigenetic regulators. These mutations frequently occur before the onset of full blown leukemia, at the pre-leukemic phase, and persist in residual disease that remains after therapeutic intervention, thus suggesting that targeting the AML epigenome may help to eradicate minimal residual disease and prevent relapse. Within the AML epigenome, lysine-specific demethylase 1 A (LSD1) is a histone demethylase that is found frequently overexpressed, albeit not mutated, in AML. LSD1 is a required constituent of critical transcription repressor complexes like CoREST and nucleosome remodeling and deacetylase (NuRD), and abrogation of LSD1 expression results in impaired self-renewal and proliferation, and increased differentiation and apoptosis in AML models and primary cells, particularly in AMLs with MLL- and AML1-rearrangements, or erythroid and megakaryoblastic differentiation block. On this basis, a number of LSD1 inhibitors have been developed in the past decade, and few of them are currently being tested in clinical trials for patients with AML, along with other malignancies. To date, the most promising application of this therapeutic strategy appears to be combination therapy of LSD1 inhibitors with all-trans retinoic acid (ATRA) to reactivate myeloid differentiation in cells that are not spontaneously susceptible to ATRA treatment. In this review, we provide an overview of LSD1 function in normal hematopoiesis and leukemia, and of the current clinical application of LSD1 inhibitors for the treatment of patients with AML

Test Methods for Image-Based Information in Next-Generation Manufacturing

Typical control designs in the process systems engineering literature have assumed that the primary sensing methodologies are traditional instruments such as thermocouples. Dig- italization is changing the landscape for manufacturing, and data-based sensing modalities (e.g., image-based sensing) are becoming of greater interest for plant control. These considerations require novel test/evaluation solutions. For example, process systems engineering researchers may wish to test image-based sensors in simulation. In this work, we provide preliminary thoughts on how image-based technologies might be evaluated via simulation for process systems

Polyomavirus BK replication in renal transplant recipients: combined monitoring of viremia and VP1 mRNA in urine

Introduction. Human polyomavirus BK (BKV) is worldwide distributed, with a seroprevalence rate of 70–90% in the adults. Following primary infection, BK remains latent in the renourinary tract as the epidemiologically most relevant latency site, and in B cell, brain, spleen and probably other tissues. Reactivation may occur in both immunocompetent subjects and immunocompromised patients. In renal transplantation, in the context of intense immunosuppression, viral replication may determine BKV-associated nephropathy (BKVAN) with interstitial nephritis and/or ureteral stenosis in 1–10% of the patients and leading to graft failure and return to haemodialysis in 30 to 80% of the cases (5). Screening of BKV replication represents the basic strategy to predict early the onset of BKVAN and may allow for earlier intervention with reduced allograft loss (3, 4). Nowadays, replication of BKV is monitored by quantification of BKV-DNA in serum and urine (2). The aim of this study was to evaluated the role of BKV VP1 mRNA in urine as a marker of viral replication in renal transplant recipients

The expression of the thyroid-stimulating hormone (TSH) receptor and the cAMP-dependent protein kinase RII beta regulatory subunit confers TSH-cAMP-dependent growth to mouse fibroblasts.

TSH activates its specific receptor in thyroid cells and induces cAMP, a robust stimulator of thyroid cell proliferation. Conversely, cAMP is a potent inhibitor of growth in mouse fibroblasts. To dissect the signals mediating cAMP-dependent growth, we have expressed in mouse fibroblasts the human thyrotropin receptor (TSHR) or a constitutively active mutant, under the control of the tetracyclin promoter. Both TSHR and cAMP levels were modulated by tetracyclin. In the presence of serum, activation of TSHR by TSH induced growth arrest. In the absence of serum, cells expressing TSHR stimulated with TSH, replicated their DNA, but underwent apoptosis. Co-expression of cAMP-dependent protein kinase (PKA) regulatory subunit type II (RIIbeta) inhibited apoptosis and stimulated the growth of cells only in the presence of TSH. Expression of RIIbeta-PKA, in the absence of TSHR, induced apoptosis, which was reversed by cAMP. Growth, stimulated by TSHR-RIIbeta-PKA in mouse fibroblasts, was also dependent on Rap1 activity, indicating cAMP-dependent growth in thyroid cells. As for the molecular mechanism underlying these effects, we found that in normal fibroblasts, TSH induced AKT and ERK1/2 only in cells expressing TSHR and RII. Similarly, activation of TSHR increased cAMP levels greatly, but was unable to stimulate CREB phosphorylation and transcription of cAMP-induced genes in the absence of RII. These data provide a simple explanation for the anti-proliferative and proliferative effects of cAMP in different cell types and indicate that RII-PKAII complements TSHR action by stably propagating robust cAMP signals in cell compartments

FACTORS RELATED TO SUBSEQUENT ADOLESCENT PREGNANCY IN THE DOMINICAN REPUBLIC

Objectives: Adolescents with subsequent pregnancies in the Dominican Republic represent a significant but poorly understood population with little available data to inform health care services. The objective of this exploratory study was to begin to characterize this important cohort. Methods: A survey of demographic items and a sexual and obstetrical history was administered to 50 adolescents with subsequent pregnancies in La Romana, Dominican Republic. Results: Most participants were married (78%) and exclusively economically dependent on their partner (72%) and nearly half (48%) stopped attending school. Twelve percent reported having intended their current pregnancy. Conclusions: Adolescents with subsequent pregnancies were dependent on partners in the form of living conditions and marriage, economic dependence and unemployment, and lack of education

DNA Damage, Homology-Directed Repair, and DNA Methylation

To explore the link between DNA damage and gene silencing, we induced a DNA double-strand break in the genome of Hela or mouse embryonic stem (ES) cells using I-SceI restriction endonuclease. The I-SceI site lies within one copy of two inactivated tandem repeated green fluorescent protein (GFP) genes (DR-GFP). A total of 2%–4% of the cells generated a functional GFP by homology-directed repair (HR) and gene conversion. However, ~50% of these recombinants expressed GFP poorly. Silencing was rapid and associated with HR and DNA methylation of the recombinant gene, since it was prevented in Hela cells by 5-aza-2′-deoxycytidine. ES cells deficient in DNA methyl transferase 1 yielded as many recombinants as wild-type cells, but most of these recombinants expressed GFP robustly. Half of the HR DNA molecules were de novo methylated, principally downstream to the double-strand break, and half were undermethylated relative to the uncut DNA. Methylation of the repaired gene was independent of the methylation status of the converting template. The methylation pattern of recombinant molecules derived from pools of cells carrying DR-GFP at different loci, or from an individual clone carrying DR-GFP at a single locus, was comparable. ClustalW analysis of the sequenced GFP molecules in Hela and ES cells distinguished recombinant and nonrecombinant DNA solely on the basis of their methylation profile and indicated that HR superimposed novel methylation profiles on top of the old patterns. Chromatin immunoprecipitation and RNA analysis revealed that DNA methyl transferase 1 was bound specifically to HR GFP DNA and that methylation of the repaired segment contributed to the silencing of GFP expression. Taken together, our data support a mechanistic link between HR and DNA methylation and suggest that DNA methylation in eukaryotes marks homologous recombined segments

An in vivo humanized model to study homing and sequestration of Plasmodium falciparum transmission stages in the bone marrow

IntroductionRecent evidence suggests that the bone marrow (BM) plays a key role in the diffusion of P. falciparum malaria by providing a “niche” for the maturation of the parasite gametocytes, responsible for human-to-mosquito transmission. Suitable humanized in vivo models to study the mechanisms of the interplay between the parasite and the human BM components are still missing.MethodsWe report a novel experimental system based on the infusion of immature P. falciparum gametocytes into immunocompromised mice carrying chimeric ectopic ossicles whose stromal and bone compartments derive from human osteoprogenitor cells.ResultsWe demonstrate that immature gametocytes home within minutes to the ossicles and reach the extravascular regions, where they are retained in contact with different human BM stromal cell types.DiscussionOur model represents a powerful tool to study BM function and the interplay essential for parasite transmission in P. falciparum malaria and can be extended to study other infections in which the human BM plays a role