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@ragimoov: #ragimoov

𝕽 𝖆 𝖌 𝖎 𝖒 𝖔 𝖔 𝖛
𝕽 𝖆 𝖌 𝖎 𝖒 𝖔 𝖔 𝖛
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Monday 31 August 2026 22:34:14 GMT
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edik_182
𓆩𝙴𝚕𝚍𝚊𝚛🧢𓆪 :
Səndən hərəkət, Allahdan bərəkət
2026-09-01 06:05:06
12
zinurabbasov2
0_Abbaszadə_1 :
Morgan Freeman çox böyük aktyordu👍🏻
2026-09-01 06:19:27
5
gulyaa_777
GulYa_777 :
Kinonun adi ne?
2026-09-01 00:43:20
1
user4874427635611
lucy :
Ne demek istedi goresen?,
2026-09-01 05:35:43
1
weliwis4
. :
bu cilips lər hardan tapağ olar
2026-09-01 07:57:30
0
maney.2000
brucewayne💲 :
ilk
2026-08-31 22:37:06
1
gulnare.muellim
Gülnarə Müəllim :
2026-09-01 03:36:54
0
ali31333222
➌➌➌𓅃 :
2026-08-31 23:15:36
0
riyaziyyat_
Riyaziyyat Hazırlığı :
👍
2026-08-31 22:41:27
0
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Other Videos

متابعة لا يك اعادة نشر يا غوالي 🤝
متابعة لا يك اعادة نشر يا غوالي 🤝
unfreeze my account #fyp #foryoupage #1millionaudition #aesthtic #poetrystatus
unfreeze my account #fyp #foryoupage #1millionaudition #aesthtic #poetrystatus


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
#LetterName #NameLetter #NameVideo #Initials #NameTrend
#LetterName #NameLetter #NameVideo #Initials #NameTrend
What is your dream car 🚗..🤲🏻😭#god #oneday #video
What is your dream car 🚗..🤲🏻😭#god #oneday #video

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