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@angelm5x: @snejanaonopka15 for #givenchy 2008 ss

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Tuesday 13 October 2026 06:13:44 GMT
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shlavsk1i
Shlavsk1i :
СКИНЬ СРОЧНО УМОЛЯЮ
2026-10-13 11:59:26
1
lookin4urn
️ :
Uuuuu u liedddd hahaha i was rightttttttttt
2026-10-13 11:03:37
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sylphoraa0
Sylphora :
ОБОЖАЮ ЭТУ ПЕСНЮ
2026-10-14 05:25:22
1
shlavsk1i
Shlavsk1i :
Клёвый показ
2026-10-13 11:59:49
1
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#القرآن الكريم # سورة الجمعة #القارئ الشيخ # امير محمد حبشي # حفظك الله ورعاك # تلاوات_خاشعة #اليوم جمعة #صلوا_على_رسول_الله_لأجل_شفاعته#
#القرآن الكريم # سورة الجمعة #القارئ الشيخ # امير محمد حبشي # حفظك الله ورعاك # تلاوات_خاشعة #اليوم جمعة #صلوا_على_رسول_الله_لأجل_شفاعته#


hEDS has traditionally been classified as a connective tissue disorder defined by joint hypermobility. This framing never fully explained why hEDS so often comes with immune dysfunction, dysautonomia, and chronic fatigue. New genetic research is reframing it as a multi-system condition. A 2025 study by Gensemer et al. in iScience (MUSC, Norris lab) performed whole-exome sequencing on 200 hEDS patients and identified a recurrent variant in KLK15, a gene active in both connective tissue and immune tissue. A knock-in mouse with the variant developed connective tissue abnormalities in tendons and heart valves alongside dysregulated cytokine signaling. A separate 2026 study by Shirvani et al. in Genes found hEDS-associated variants enriched across three systems: collagen biosynthesis, HLA/immune pathways, and mitochondrial function. KLK15 is described as a contributor, not a confirmed single cause. The variant was found in roughly a third of patients, and hEDS remains genetically complex. This research does not yet enable a genetic test for hEDS, and the 2017 clinical criteria remain the standard for diagnosis. The multi-system genetic paper used machine learning on a single cohort and needs replication. I’m not a doctor, just sharing research I find interesting. Sources: Gensemer et al. (2025). iScience. DOI: 10.1016/j.isci.2025.113343 Shirvani et al. (2026). Genes. DOI: 10.3390/genes17020211 #heds #ehlersdanlos #chronicillness #hypermobileehlersdanlossyndrome
hEDS has traditionally been classified as a connective tissue disorder defined by joint hypermobility. This framing never fully explained why hEDS so often comes with immune dysfunction, dysautonomia, and chronic fatigue. New genetic research is reframing it as a multi-system condition. A 2025 study by Gensemer et al. in iScience (MUSC, Norris lab) performed whole-exome sequencing on 200 hEDS patients and identified a recurrent variant in KLK15, a gene active in both connective tissue and immune tissue. A knock-in mouse with the variant developed connective tissue abnormalities in tendons and heart valves alongside dysregulated cytokine signaling. A separate 2026 study by Shirvani et al. in Genes found hEDS-associated variants enriched across three systems: collagen biosynthesis, HLA/immune pathways, and mitochondrial function. KLK15 is described as a contributor, not a confirmed single cause. The variant was found in roughly a third of patients, and hEDS remains genetically complex. This research does not yet enable a genetic test for hEDS, and the 2017 clinical criteria remain the standard for diagnosis. The multi-system genetic paper used machine learning on a single cohort and needs replication. I’m not a doctor, just sharing research I find interesting. Sources: Gensemer et al. (2025). iScience. DOI: 10.1016/j.isci.2025.113343 Shirvani et al. (2026). Genes. DOI: 10.3390/genes17020211 #heds #ehlersdanlos #chronicillness #hypermobileehlersdanlossyndrome
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#disturbing #accident #supernatural #horror #scary
#ghosthunter #paranormal #ghost #hillhouse #ghosthunting
#ghosthunter #paranormal #ghost #hillhouse #ghosthunting
#pashtosong #viral #fyp #foryoupage #foryou
#pashtosong #viral #fyp #foryoupage #foryou

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