12 research outputs found
Fashion History Through the Story of Dolls
A new mademoiselle has arrived! A stately English lady rustles up as rapidly as her fourteenth century dignity will allow her, to peek at the petite model beautifully dressed in the latest mode of the French court
The Iowa Homemaker vol.19, no.7
The Fashion World, page 1
Highlights of Leather, page 2
Inside Story of Costume Creation, page 3
Sally Cures Spring Fever, page 4
Designers Inspire Clothes-Conscious Coed, page 6
Trim Togs for Oomph, page 7
Fur – A Costume Climax, page 8
Fashion History Through the Story of Dolls, page 9
What’s New In Home Economics, page 10
Design Your Own, page 12
Hosiery Goes Modern, page 13
Research Brings Better Buymanship, page 14
Alums in the News, page 15
Behind Bright Jackets, page 16
Discover Your Jewelry Personality, page 17
Fashion Finds a la francais, page 18
From Journalistic Spindles, page 19
Biography of a Home Economist, page 2
Stroke genetics informs drug discovery and risk prediction across ancestries
Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries
Stroke genetics informs drug discovery and risk prediction across ancestries
Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p
Fashion History Through the Story of Dolls
A new mademoiselle has arrived! A stately English lady rustles up as rapidly as her fourteenth century dignity will allow her, to peek at the petite model beautifully dressed in the latest mode of the French court.</p
The Iowa Homemaker vol.19, no.7
The Fashion World, page 1
Highlights of Leather, page 2
Inside Story of Costume Creation, page 3
Sally Cures Spring Fever, page 4
Designers Inspire Clothes-Conscious Coed, page 6
Trim Togs for Oomph, page 7
Fur – A Costume Climax, page 8
Fashion History Through the Story of Dolls, page 9
What’s New In Home Economics, page 10
Design Your Own, page 12
Hosiery Goes Modern, page 13
Research Brings Better Buymanship, page 14
Alums in the News, page 15
Behind Bright Jackets, page 16
Discover Your Jewelry Personality, page 17
Fashion Finds a la francais, page 18
From Journalistic Spindles, page 19
Biography of a Home Economist, page 20</p
Interferon alpha extends the survival of human myeloma cells through an upregulation of the Mcl-1 anti-apoptotic molecule
International audienceWe have recently reported that Mcl-1, an anti-apoptotic member of the Bcl-2 family, is upregulated by interleukin (IL)-6 in human myeloma cells through the janus kinase/signal transducers and activators of transduction (JAK/STAT) pathway. In the current study, we have explored the effects of interferon (IFN)-alpha, a cytokine which has been shown to increase myeloma cell survival. Our results demonstrate that IFN-alpha potently upregulates Mcl-1 on both myeloma cell lines and purified native myeloma cells. Of note, this upregulation is not due to an induction of an IL-6 autocrine loop. Furthermore, we showed that IL-6 and IFN-alpha had no additive effect on Mcl-1 upregulation, suggesting that both cytokines act through a common mechanism. Finally, the analysis of signalling transduction pathways strongly suggests that Mcl-1 upregulation induced by IFN-alpha depends on STAT3 activation. Altogether, our data show that IFN-alpha has an IL-6-like effect on human myeloma cells and suggest that it could be deleterious in some patients