13 research outputs found
Codes of Commitment to Crime and Resistance: Determining Social and Cultural Factors over the Behaviors of Italian Mafia Women
This article categorizes thirty-three women in four main Italian Mafia groups and explores social and cultural behaviors of these women. This study introduces the feminist theory of belief and action. The theoretical inquiry investigates the sometimes conflicting behaviors of women when they are subject to systematic oppression. I argue that there is a cultural polarization among the categorized sub-groups. Conservative radicals give their support to the Mafia while defectors and rebels resist the Mafia. After testing the theory, I assert that emancipation of women depends on the strength of their beliefs to perform actions against the Mafiosi culture
Mechanisms that clear mutations drive field cancerization in mammary tissue
Oncogenic mutations are abundant in the tissues of healthy individuals, but rarely form tumours1â3. Yet, the underlying protection mechanisms are largely unknown. To resolve these mechanisms in mouse mammary tissue, we use lineage tracing to map the fate of wild-type and Brca1â/â;Trp53â/â cells, and find that both follow a similar pattern of loss and spread within ducts. Clonal analysis reveals that ducts consist of small repetitive units of self-renewing cells that give rise to short-lived descendants. This offers a first layer of protection as any descendants, including oncogenic mutant cells, are constantly lost, thereby limiting the spread of mutations to a single stem cell-descendant unit. Local tissue remodelling during consecutive oestrous cycles leads to the cooperative and stochastic loss and replacement of self-renewing cells. This process provides a second layer of protection, leading to the elimination of most mutant clones while enabling the minority that by chance survive to expand beyond the stem cell-descendant unit. This leads to fields of mutant cells spanning large parts of the epithelial network, predisposing it for transformation. Eventually, clone expansion becomes restrained by the geometry of the ducts, providing a third layer of protection. Together, these mechanisms act to eliminate most cells that acquire somatic mutations at the expense of driving the accelerated expansion of a minority of cells, which can colonize large areas, leading to field cancerization
A new psychology of women : gender, culture and ethnicity
xxi, 490 p. : ill ; 23 c
A longitudinal study of the reporting of emotional and somatic symptoms during and after pregnancy
One hundred and eight pregnant women, most of their husbands and a comparison group of non-expectant parents were recruited for a long-term study which involved responding to a 55-item Symptom Checklist (SCL) and the Beck Depression Inventory three times during pregnancy and once during the first postpartum month. Responses to the SCL were factor analysed, and the four groups were then compared on their factor scores as well as their scores on the Beck Depression Inventory (BDI) using discriminant analysis and trend analysis. The discriminant analyses were done twice: once using all the data provided by all subjects and once using only subjects with no missing data. At each measurement period, the pregnant women were distinguished from the other groups by a different factor of the SCL: at 3-5 months, it was 'Feeling Sick': at 6-8 months, it was 'Feeling Overweight'; at 9 months, it was 'Feeling Overweight/Physical Stress'; and at postpartum, it was 'Physical Stress'. Also, trend analysis showed a significant tendency for the scores of pregnant women on the SCL 'Negative Emotional State', factor and on the BDI to increase over time, in contrast to those of the other groups.
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Mechanisms that clear mutations drive field cancerization in mammary tissue
Acknowledgements: We thank the laboratories of van Rheenen and Scheele for critically reading the manuscript, and the Netherlands Cancer Institute (NKI) Animal facility, NKI BioImaging facility and the NKI genomics core facility for their technical support. This work was supported by the Boehringer Ingelheim Foundation (PhD Fellowship to C.L.G.J.S.), a Federation of European Biochemical Societies excellence award (to C.L.G.J.S.), the Research Foundation Flanders (PhD grant fundamental research no. 11L7222N to M.C.), EMBO (postdoctoral fellowship grant nos. ALTF 452-2019 to H.A.M. and ALTF 1035-2020 to C.L.G.J.S.) and the European Research Council (consolidator grant no. 648804 to J.v.R.), the Doctor Josef Steiner Foundation (to J.v.R.), the Netherlands Organization of Scientific Research (NWO) (Vici grant no. 09150182110004 to J.v.R., and Veni grant no. 09150161910151 to H.A.M.) and a joint grant of the Cancer Research UK and KWF Kankerbestrijding (ref. C38317/A24043). B.D.S. acknowledges funding from the Royal Society E.P. Abraham Research Professorship (grant nos. RP\R1\180165 and RSRP\R\231004) and Wellcome (grant nos. 098357/Z/12/Z and 219478/Z/19/Z). We regret that we could not cite all the important contributions in this field due to the constraint of being limited to citing only 60 studies. This research was funded, in part, by the Wellcome Trust (098357/Z/12/Z and 219478/Z/19/Z). For the purpose of Open Access, the authors have applied a CC BY public copyright license to any Author Accepted Manuscript version arising from this submission.AbstractOncogenic mutations are abundant in the tissues of healthy individuals, but rarely form tumours1â3. Yet, the underlying protection mechanisms are largely unknown. To resolve these mechanisms in mouse mammary tissue, we use lineage tracing to map the fate of wild-type and Brca1â/â;Trp53â/â cells, and find that both follow a similar pattern of loss and spread within ducts. Clonal analysis reveals that ducts consist of small repetitive units of self-renewing cells that give rise to short-lived descendants. This offers a first layer of protection as any descendants, including oncogenic mutant cells, are constantly lost, thereby limiting the spread of mutations to a single stem cell-descendant unit. Local tissue remodelling during consecutive oestrous cycles leads to the cooperative and stochastic loss and replacement of self-renewing cells. This process provides a second layer of protection, leading to the elimination of most mutant clones while enabling the minority that by chance survive to expand beyond the stem cell-descendant unit. This leads to fields of mutant cells spanning large parts of the epithelial network, predisposing it for transformation. Eventually, clone expansion becomes restrained by the geometry of the ducts, providing a third layer of protection. Together, these mechanisms act to eliminate most cells that acquire somatic mutations at the expense of driving the accelerated expansion of a minority of cells, which can colonize large areas, leading to field cancerization.</jats:p