Fussy girls and chattering women – the construct and subordination of femininity in preschool teacher training

In Sweden, as in Western countries generally, most preschool teachers are women. This fact sometimes leads to the assumption that preschools are “feminine”, and that this might be bad for boys. We challenge this assumption. Using a gender critical approach we have studied preschool student teachers. “Femininity” might be used as a rhetorical and demeaning stereotype by them. Women and femininity however, are not interchangeable concepts. Failure to acknowledge this can pave the way for subtle sexism against girls and women. Our argument is supported by ethnographic observations and interviews with student teachers. By means of a Foucauldian genealogical analysis we uncover the conditions of possibility for two long-lasting feminine stereotypes. One stereotype argues that young girls should never fuss. The other claims that women are chattering gossipers. Our study shows that these archaic notions persist in Swedish preschool teacher training, despite its long tradition of work for gender equality.     

冠心病血瘀证遗传相关的差异基因筛选及其功能路径分析

目的 探讨冠心病(coronary heart disease,CHD)血瘀证遗传相关的差异基因功能及目标通路。方法 以家系CHD血瘀证者(A组)及家系CHD非血瘀证者(B组)、家系非CHD血瘀证者(C组)、家系健康人(D组)、非家系CHD血瘀证者(E组)、非家系健康人(F组)为研究对象,应用基因芯片技术比较A组与B、C、D、E组,以及D组与F组的差异基因表达谱;通过基因本体论(gene ontology,GO)分析阐释差异基因的分子功能;通过BioCarta及KEGG网站寻找差异基因所在通路,应用超几何分布统计学方法分析筛选出有意义的目标通路,并用实时荧光定量RT PCR对差异基因进行验证。结果 (1)通过对基因芯片数据的筛选(差异倍数≥3),发现家系CHD血瘀证差异基因表达主要涉及趋化因子、白介素细胞因子、补体系统、基质金属蛋白酶系、成纤维细胞生长因子、内皮细胞黏附因子等。(2)通过相关差异基因(P<0.05)GO分析,找到与CHD血瘀证相关的差异基因的分子功能。(3)经过BioCarta及KEGG通路分析,发现家系CHD血瘀证与遗传相关的差异基因中差异有统计学意义(P<0.05)的目标通路主要涉及到炎症、斑块形成、内皮损伤等方面。经实时荧光定量RT-PCR反应验证了基因芯片准确可靠。结论 CHD血瘀证遗传相关的差异基因与炎症、斑块形成及血管内皮损伤密切相关。     

Seeing the Wood for the Trees: A Minimal Reference Phylogeny for the Human Y Chromosome

During the last few decades, a wealth of studies dedicated to the human Y chromosome and its DNA variation, in particular Y‐chromosome single‐nucleotide polymorphisms (Y‐SNPs), has led to the construction of a well‐established Y‐chromosome phylogeny. Since the recent advent of new sequencing technologies, the discovery of additional Y‐SNPs is exploding and their continuous incorporation in the phylogenetic tree is leading to an ever higher resolution. However, the large and increasing amount of information included in the “complete” Y‐chromosome phylogeny, which now already includes many thousands of identified Y‐SNPs, can be overwhelming and complicates its understanding as well as the task of selecting suitable markers for genotyping purposes in evolutionary, demographic, anthropological, genealogical, medical, and forensic studies. As a solution, we introduce a concise reference phylogeny whereby we do not aim to provide an exhaustive tree that includes all known Y‐SNPs but, rather, a quite stable reference tree aiming for optimal global discrimination capacity based on a strongly reduced set that includes only the most resolving Y‐SNPs. Furthermore, with this reference tree, we wish to propose a common standard for Y‐marker as well as Y‐haplogroup nomenclature. The current version of our tree is based on a core set of 417 branch‐defining Y‐SNPs and is available online at http://www.phylotree.org/Y .     

Estimating Human Inbreeding Coefficients: Comparison of Genealogical and Marker Heterozygosity Approaches

We have used genealogies and genomic polymorphisms to estimate individual inbreeding coefficients (F) in 50 subjects with an expected range (based on recent genealogies) of F from 0.0 to 0.0625. The estimates were based on two approaches, using genotypes respectively from 410 microsatellite markers (410‐STR panel) and from 10,000 SNPs (10K‐SNP panel). The latter was performed in a sub‐sample of 15 individuals. We concluded that for both marker panels measures of inbreeding based on the excess of homozygosity over Hardy‐Weinberg expectation were not closely correlated with 4‐5 generation genealogical F‐values. For the 10K‐SNP panel we found two alternative measures which correlated more closely with F, based respectively on standard errors and on paired homozygosity of nearby SNPs over distances of 2‐4 cM. We propose an empirical method for estimating standard errors and hence individual F‐values, based on the variation between individual autosomes. This method could provide useful estimates of average F‐values for groups of individuals in population‐based studies of the effects of inbreeding/homozygosity on quantitative traits.     

Was the C282Y mutation an Irish Gaelic mutation that the Vikings helped disseminate?*

The HLA‐related hemochromatosis mutation C282Y is thought to have originated in Ireland in a person with HLA‐A3‐B14 and was spread by Vikings. Irish people with two HLA‐A3 alleles had a high risk of hemochromatosis. In this study, from west Sweden, we wanted to test these hypotheses. Methods: HFE mutations in controls, bone marrow donors with HLA‐A3/A3 and patients with hemochromatosis. HLA haplotypes, extended haplotype analysis and pedigree studies. Results: The allelic C282Y frequency 0.04, (CI 0.01–0.07) was lower (P < 0.001) in Sweden than in Ireland 0.10 (CI 0.08–0.11), and Swedish bone marrow donors with HLA‐A3/A3 (n = 77) had a low risk of hemochromatosis. HLA haplotypes available from 239/262 (91.5%) proband patients homozygous for C282Y showed a dominance of A3‐B7 and A3‐B14 both in linkage disequilibrium with controls (P < 0.001). Pedigree studies extended into the 17th century supported a local founder effect of A3‐B14 in the county of Bohuslän. The A3‐B14 haplotype may well be the original and A3‐B7 the result of centromeric recombinations. The haplotype diversity and recombination events were not different from a Celtic series. These findings do not support the hypothesis of the C282Y mutation being of an Irish Celtic origin. Conclusions: The C282Y frequency shows a west to east decline from Ireland through the north of Europe. Vikings may have been involved in the spread of C282Y, but the mutation is probably older and may have been spread in Europe by earlier seafarers.     

HLA haplotype map of river valley populations with hemochromatosis traced through five centuries in Central Sweden

Background: The hemochromatosis mutation, C282Y of the HFE gene, seems to have originated from a single event which once occurred in a person living in the north west of Europe carrying human leukocyte antigen (HLA)‐A3‐B7. In descendants of this ancestor also other haplotypes appear probably caused by local recombinations and founder effects. The background of these associations is unknown. Isolated river valley populations may be fruitful for the mapping of genetic disorders such as hemochromatosis. In this study, we try to test this hypothesis in a study from central Sweden where the haplotyope A1‐B8 was common. Methods: HLA haplotypes and HFE mutations were studied in hemochromatosis patients with present or past parental origin in a sparsely populated (1/km²) rural district (n = 8366 in the year of 2005), in central Sweden. Pedigrees were constructed from the Swedish church book registry. Extended haplotypes were studied to evaluate origin of recombinations. Results: There were 87 original probands, 36 females and 51 males identified during 30 yr, of whom 86% carried C282Y/C282Y and 14% C282Y/H63D. Of 32 different HLA haplotypes A1‐B8 was the most common (34%), followed by A3‐B7 (16%), both in strong linkage disequilibrium with controls, (P < 0.001). Twenty‐nine different families with A1‐B8 had a common founder origin 15 generations ago in small bottleneck populations of the late 16th century. A second A1‐B8 founder born 1655 was of Norwegian origin. Most of the A3 carriers (n = 26) had a common founder origin 16 generations ago in an even smaller nearby river valley. A fourth founder family carrying HLA‐A2 seems to have originated from a recombination along the descendant lines from the A3 ancestor supported by extended haplotype studies. A1‐haplotypes with alleles at the B locus different from B8 had a similar recombination origin as HLA‐A2 alleles and a common founder origin 11 generations ago. The intergenerational time interval averaged 35.5 ± 7.9 yr in men and 31.9 ± 5.9 in females. Conclusions: River valley populations may contain HLA haplotypes reflecting their demographic history. This study has demonstrated that the resistance against recombinations between HLA‐A and HFE make HLA haplotypes excellent markers for population movements. Founder effects and genetic drift from bottleneck populations (surviving the plague?) may explain the commonness of the mutation in central Scandinavia. The intergenerational time difference >30 yr was greater than expected and means that the age of the original mutation may be underestimated.     

The number of genotypic assignments on a genealogy I. The method and simple examples

This paper demonstrates how the number of possible genotypicassignments consistent with the rules of Mendelian geneticsand with any known phenotypes can be calculated for an arbitrarygenealogy. This is of interest both in the context of the usesof the Metropolis algorithm for pedigree analysis and in itsown right. Bounds on the number of states for certain regularand random genealogies are also obtained, and further resultswill be given in a later paper.     

Family distances can reveal hidden consanguinity

Family distances, defined as summary measures of all possible geographic distances between birthplaces of paternal ancestors and birthplaces of maternal ancestors in a given generation, were compared in patients with autosomal recessive disorders and patients with Down's syndrome. In general, family distances in Down's syndrome patients were twice the family distances in patients with autosomal recessive disorders, even after the exclusion of rare disorders or cases with overt consanguinity. In modern, Western European societies grandparental and great-grandparental family distances may be more appropriate measures of the effect of population structure than parental distance or parental consanguinity.     

Problematizing special observation in psychiatry: Foucault, archaeology, genealogy, discourse and power/knowledge

Special observation by mental health professionals is the recommended approach for those people deemed as at risk or risky. Recent research and academic writing have challenged the benefits of observing people/patients who are defined as 'at risk', and a more human engagement process is being recommended. Despite this assault, practice has not changed substantively, suggesting a need for a thorough exploration and questioning of the practices and process. The paper outlines three Foucaultian approaches to historical analysis. It applies aspects of Foucault's archaeology/genealogy, discourse and power/knowledge to explore the practices of special observation as a means of controlling risk, especially suicide risk. We identify the regulatory function of the 'gaze', professional codes and government policy in relation to restricting professional practices. We argue that observation can be related to moral therapy, wherein the person relinquishes madness for responsibility through a disciplinary process and, in governing risk, a 'professional industry' is created. The regulation of statements about people with mental health issues are exposed and related to what can be said and done by professionals. Finally, we look at productive power in relation to observation, and how it is intimately related to resistance. We conclude with 'soft' recommendations for practice discursively produced through the writing of the paper.