Rights Myopia in Child Welfare

For decades, legal scholars have debated the proper balance of parents\u27 rights and children\u27s rights in the child welfare system. This Article argues that the debate mistakenly privileges rights. Neither parents\u27 rights nor children\u27s rights serve families well because, as implemented, a solely rights-based model of child welfare does not protect the interests of parents or children. Additionally, even if well-implemented, the model still would not serve parents or children because it obscures the important role of poverty in child abuse and neglect and fosters conflict rather than collaboration between the state and families. In lieu of a solely rights-based model, this Article proposes a problem-solving model for child welfare and explores one embodiment of such a model, family group conferencing. This Article concludes that a problem-solving model holds significant potential to address many of the profound theoretical and practical shortcomings of the current child welfare system

Emergency Department as an epidemiological observatory of Human Mobility: the experience of the Moroccan population

We conducted a retrospective study of the accesses to the Emergency Department registered from January 2000 to December 2014 in 5 major hospitals in the Metropolitan Area of Rome. We extrapolated data relating to patients of Moroccan origin from about 5 million total accesses, so we compared with Italians data which, in the same period, came to ED. The Moroccan population is distinguished by a larger number of diagnoses belonging to the ICD-9 code of Infectious Diseases and, more precisely, to Respiratory Infectious Diseases. There are also no differences in the assignment of such diagnoses to Moroccans with Italian citizenship, and this led to think that this could play an important role in the use of the ED and moreover that enrollment to the National Health Service may reduce its inappropriate use. Regarding to Degenerative Disorders, the result of our analysis is quite emblematic, showing that the accesses to the ED is due to Cardiovascular Diseases: 6.33% of Italians' accesses against 1.81% of Moroccans and 2.36% of Moroccans with Italian citizenship. The main explanation for this difference is, obviously, due to the age of the population: about 60% of Moroccans who accessed to ED was less than 40 years old. It is interesting how, in the field of ​​Cardiovascular Diseases, Moroccans have a lower percentage of diagnosis compared to Italians for acute diseases and a greater percentage of diagnoses for chronic diseases, suggesting once again that accesses to ED for migrants often is due to the inability to use the general services of the National Health Service. In conclusion, from the point of view of the Emergency Department, Migration Medicine still has Infectious Diseases as the main reason for access. Degenerative Disorders remain a prerogative of the Italians, but we could certainly assume that the Moroccan population would develop at some point with the aging

Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms

Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2V617F-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10−10) and rs2201862 (MECOM; meta-analysis P=1.96 × 10−9). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2V617F-positive cases. rs9376092 has a stronger effect in JAK2V617F-negative cases with CALR and/or MPL mutations (Breslow–Day P=4.5 × 10−7), whereas in JAK2V617F-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ2 P=7.3 × 10−7). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype

Asphodelus fistulosus L. (Liliaceae) subespontáneo en la Argentina (nota breve)

p.113-11

MARIMO cells harbor a CALR mutation but are not dependent on JAK2/STAT5 signaling.

Work in the Green lab is supported by Leukemia and Lymphoma Research, Cancer Research UK, the NIHR Cambridge Biomedical Research Centre, the Cambridge Experimental Cancer Medicine Centre, and the Leukemia and Lymphoma Society of America. WW is supported by the Austrian Science Foundation (J 3578-B21). JN is supported by a Kay Kendall Leukaemia Clinical Fellowship.This is the final published version. It first appeared at http://www.nature.com/leu/journal/vaop/ncurrent/full/leu2014285a.html

A data-driven network model of primary myelofibrosis: transcriptional and post-transcriptional alterations in CD34+ cells

microRNAs (miRNAs) are relevant in the pathogenesis of primary myelofibrosis (PMF) but our understanding is limited to specific target genes and the overall systemic scenario islacking. By both knowledge-based and ab initio approaches for comparative analysis of CD34+ cells of PMF patients and healthy controls, we identified the deregulated pathways involving miRNAs and genes and new transcriptional and post-transcriptional regulatory circuits in PMF cells. These converge in a unique and integrated cellular process, in which the role of specific miRNAs is to wire, co-regulate and allow a fine crosstalk between the involved processes. The PMF pathway includes Akt signaling, linked to Rho GTPases, CDC42, PLD2, PTEN crosstalk with the hypoxia response and Calcium-linked cellular processes connected to cyclic AMP signaling. Nested on the depicted transcriptional scenario, predicted circuits are reported, opening new hypotheses. Links between miRNAs (miR-106a-5p, miR-20b-5p, miR-20a-5p, miR-17-5p, miR-19b-3p and let-7d-5p) and key transcription factors (MYCN, ATF, CEBPA, REL, IRF and FOXJ2) and their common target genes tantalizingly suggest new path to approach the disease. The study provides a global overview of transcriptional and post-transcriptional deregulations in PMF, and, unifying consolidated and predicted data, could be helpful to identify new combinatorial therapeutic strategy. Interactive PMF network model: http://compgen.bio.unipd.it/pmf-net/

Targeted cancer exome sequencing reveals recurrent mutations in myeloproliferative neoplasms

With the intent of dissecting the molecular complexity of Philadelphia-negative myeloproliferative neoplasms (MPN), we designed a target enrichment panel to explore, using next-generation sequencing (NGS), the mutational status of an extensive list of 2,000 cancer-associated genes and microRNAs. The genomic DNA of granulocytes and in-vitro-expanded CD3+ T-lymphocytes, as a germline control, was target-enriched and sequenced in a learning cohort of 20 MPN patients using Roche 454 technology. We identified 141 genuine somatic mutations, most of which were not previously described. To test the frequency of the identified variants, a larger validation cohort of 189 MPN patients was additionally screened for these mutations using Ion Torrent AmpliSeq NGS. Excluding the genes already described in MPN, for 8 genes (SCRIB, MIR662, BARD1, TCF12, FAT4, DAP3, POLG, and NRAS), we demonstrated a mutation frequency between 3 and 8%. We also found that mutations at codon 12 of NRAS (NRASG12V and NRASG12D) were significantly associated, for primary myelofibrosis (PMF), with highest DIPSS-plus score categories. This association was then confirmed in 66 additional PMF patients composing a final dataset of 168 PMF showing an NRAS mutation frequency of 4.7%, which was associated with a worse outcome, as defined by the DIPSS plus score

Triplet vs doublet lenalidomide-containing regimens for the treatment of elderly patients with newly diagnosed multiple myeloma

Lenalidomide-dexamethasone improved outcome in newly diagnosed elderly multiple myeloma patients. We randomly assigned 662 patients who were age \u202165 years or transplantation-ineligible to receive induction with melphalan-prednisone-lenalidomide (MPR) or cyclophosphamide-prednisone-lenalidomide (CPR) or lenalidomide plus lowdose dexamethasone (Rd). The primary end point was progression-free survival (PFS) in triplet (MPR and CPR) vs doublet (Rd) lenalidomide-containing regimens. After a median follow-up of 39 months, the medianPFSwas22 months for the triplet combinations and 21 months for the doublet (P 5 .284). The median overall survival (OS) was not reached in either arms, and the 4-year OS was 67% for the triplet and 58% for the doublet arms (P 5 .709). By considering the 3 treatment arms separately, no difference in outcome was detected among MPR, CPR, and Rd. The most common grade \u20213 toxicity was neutropenia: 64% in MPR, 29% in CPR, and 25% in Rd patients (P < .0001). Grade \u20213 nonhematologic toxicities were similar among arms and were mainly infections (6.5% to 11%), constitutional (3.5% to 9.5%), and cardiac (4.5% to 6%), with no difference among the arms. In conclusion, in the overall population, the alkylator-containing tripletsMPRandCPRwere not superior to the alkylator-free doublet Rd, which was associated with lower toxicit