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@cngmtc: Áo polo cổ V form Cleanfit tôn vai tôn bắp tay vải co giãn chống nhăn #vintage #xuhuong #aothun #trendinh #fyt

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Tuesday 28 July 2026 00:22:27 GMT
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cuong15072000
CườnG Đang Xây kênh Tiktok :
1m8-85kg Ko bon chen đc 🥴
2026-08-02 13:50:22
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حبيتَ ايامي بيك 🥹❣️. #اغاني #اليسا
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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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