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za dan gui hannah i hoffman breanna m titchen yutaro tanaka erica pimenta theodora pappa laura valderrabano kevin bi riaz gillani lauren brais erin shannon jason l hornick jihye park jennifer chan eliezer m van allen dapagliflozin attenuates progression from prefrailty to frailty in patients with hypertension and chronic kidney disease pasquale mone davide viggiano antonella pansini maria virginia soldovieri giada sabatelli valeria visco gaetano macina eugenio boccalone michele ciccarelli giuseppe martinelli marco di mauro carmine vecchione maria morgante fahimeh varzideh germano guerra gaetano santulli pasquale mone davide viggiano antonella pansini maria virginia soldovieri giada sabatelli valeria visco gaetano macina eugenio boccalone michele ciccarelli giuseppe martinelli marco di mauro carmine vecchione maria morgante fahimeh varzideh germano guerra gaetano santulli view text pdf clinical research and public health dapagliflozin attenuates progression from prefrailty to frailty in patients with hypertension and chronic kidney disease text pdf abstract background chronic kidney disease ckd and hypertension share common pathophysiological pathways contributing to vascular damage endothelial dysfunction and physical decline particularly in older adults with prefrailty to evaluate the relationship among renal injury physical performance and frailty progression in hypertensive older adults with ckd and assess whether dapagliflozin associates with reduced frailty progression we designed the study dapa fortress dapagliflozin and frailty progression in hypertension and chronic kidney disease methods we enrolled 135 prefrail hypertensive patients with ckd aged 65 years and followed them for 1 year after coarsened exact matching our balanced cohort had 105 patients 52 dapagliflozin associations between albuminuria estimated glomerular filtration rate egfr and physical performance were analyzed using correlation and regression models effect of dapagliflozin on frailty progression was evaluated using multivariable logistic regression results a significant inverse association between gait speed and albuminuria r2 0 48 p 0 0001 and significant positive linear association between gait speed and egfr r2 0 18 p 0 0001 were observed patients with egfr 60 ml min 1 73 m2 exhibited significantly worse physical performance than those with higher egfr p 0 0003 in adjusted analyses receiving dapagliflozin was independently associated with lower odds of progressing to frailty at 1 year or 0 130 ci 0 045 0 381 p 0 001 conclusion in older hypertensive patients with ckd greater renal injury is associated with worse physical performance while dapagliflozin use reduces the risk of frailty progression these findings indicate a potential protective role of sodium glucose cotransporter 2 inhibition in mitigating functional decline in this high risk population funding nih national heart lung and blood institute r01 hl146691 national institute of diabetes and digestive and kidney diseases r01 dk123259 american heart association aha 24ipa1268813 aha 22 915561 aha 24 1195524 authors pasquale mone davide viggiano antonella pansini maria virginia soldovieri giada sabatelli valeria visco gaetano macina eugenio boccalone michele ciccarelli giuseppe martinelli marco di mauro carmine vecchione maria morgante fahimeh varzideh germano guerra gaetano santulli nuclear cgas governs transcription to control lipid metabolism tumor growth and therapy response yu deng matthew j niederhuber zhichuan zhu austin j hepperla le yu quentin hahn joshua hartsell tooba rashid piotr a mieczkowski hemant kelkar jeremy m simon yanqiong zhang alessandra livraghi butrico meredith j zeller joseph g c kennedy jazmin f depriest jiong li yan zhang xing qiu h ümit kaniskan jian jin corbin d jones laura e herring douglas h phanstiel xiaojing liu jesse r raab brian d strahl pengda liu yu deng matthew j niederhuber zhichuan zhu austin j hepperla le yu quentin hahn joshua hartsell tooba rashid piotr a mieczkowski hemant kelkar jeremy m simon yanqiong zhang alessandra livraghi butrico meredith j zeller joseph g c kennedy jazmin f depriest jiong li yan zhang xing qiu h ümit kaniskan jian jin corbin d jones laura e herring douglas h phanstiel xiaojing liu jesse r raab brian d strahl pengda liu view text pdf nuclear cgas governs transcription to control lipid metabolism tumor growth and therapy response text pdf abstract cyclic gmp amp synthase cgas is a cytosolic dna sensor critical for host defense against microbial infections to prevent aberrant activation nuclear cgas is restrained by nucleosome tethering or by barrier to autointegration factor mediated restriction of its access to dna however its physiological roles beyond enzymatic suppression in the nucleus remain poorly understood here we present a genome wide map of cgas chromatin localization in human cells and unexpectedly find its binding beyond nucleosome tethering where cgas is recruited to chromatin by ap 1 transcription factors via a potentially previously uncharacterized transactivation domain integrated cut run rna seq and metabolomics analyses reveal that cgas transcriptionally regulates cholesterol homeostasis mechanistically cgas promotes lgals3 transcription which inhibits acaa2 activity to suppress fatty acid oxidation and acetyl coa production thereby lowering intracellular cholesterol levels reduced cholesterol lowers plasma membrane phosphatidylinositol 3 4 5 triphosphate pi 3 4 5 p3 levels and decreases mtor complex 2 mtorc2 activation in contrast cgas depletion results in cholesterol accumulation and elevated pi 3 4 5 p3 driving mtorc2 akt signaling promoting xenografted tumor growth and conferring resistance to dna damaging agents in vivo the elevated hepatic cholesterol levels observed in cgas mice were largely reversed by inhibition of akt but not sting whereas cgas deficiency had minimal effects on lung physiology collectively our findings uncover an unexpected role for nuclear cgas in orchestrating a transcriptional program that links lipid metabolism to cell proliferation stress response and cholesterol homeostasis in liver authors yu deng matthew j niederhuber zhichuan zhu austin j hepperla le yu quentin hahn joshua hartsell tooba rashid piotr a mieczkowski hemant kelkar jeremy m simon yanqiong zhang alessandra livraghi butrico meredith j zeller joseph g c kennedy jazmin f depriest jiong li yan zhang xing qiu h ümit kaniskan jian jin corbin d jones laura e herring douglas h phanstiel xiaojing liu jesse r raab brian d strahl pengda liu b cell depletion improves therapeutic index of combination checkpoint blockade in patients with advanced melanoma kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar view text pdf clinical research and public health b cell depletion improves therapeutic index of combination checkpoint blockade in patients with advanced melanoma text pdf abstract background combined checkpoint blockade ccb of programmed death 1 pd 1 and cytotoxic t lymphocyte associated protein 4 ctla 4 is highly active in melanoma but limited by significant morbidity from immune related adverse events iraes effective strategies to prevent ccb mediated iraes are lacking methods patients with advanced melanoma were randomly assigned to receive standard of care ipilimumab and nivolumab alone arm a ipi nivo n 7 or with one cycle of rituximab arm b ipi nivo rituximab n 7 results patients receiving ipi nivo rituximab experienced lower rates of greater than grade 3 g3 iraes 14 versus 57 and superior g3 irae free survival compared with those in ipi nivo arm 2 year g3 irae free survival 86 versus 29 p 0 01 without adverse impact on tumor regression or survival g3 hypersensitivity reactions to rituximab 43 in arm b prompted trial closure rituximab depleted pretherapy activated naive b cells linked to autoimmunity and enhanced ccb mediated induction of myeloid inflammation and cxcl13 icos cd4 t cells conclusion b cell depletion favorably modulates ccb mediated immune activation and may reduce irae risk trial registration clinicaltrials gov nct03719131 funding nih ca238471 ar077926 ca289978 and ca290302 authors kavita m dhodapkar antonio matera alyssa m duffy azmain taz renee julia manalo melinda yushak ragini kudchadkar david h lawson madhav v dhodapkar krox20 marks sebaceous gland stem cells and regulates their differentiation to maintain skin oil balance yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le view text pdf krox20 marks sebaceous gland stem cells and regulates their differentiation to maintain skin oil balance text pdf abstract oil producing sebaceous glands sgs attached to the upper middle portion of hair follicles are indispensable for maintaining skin hydration and their dysfunction leads to dry skin however the molecular mechanisms underlying regulation of sg stem cells remain largely unknown we identified transcription factor krox20 as a marker of sg stem cells that sustains their stemness throughout sg morphogenesis and homeostasis we developed an inducible mouse model in which ablation of krox20 positive cells causes sg loss and rapidly and robustly induces dry flaky alopecia symptoms following induction this model termed xeroflacia xero xerosis fla flaky cia alopecia provides a tool for studying the biology of dry skin furthermore we found that krox20 directly regulates notch1 transcription to orchestrate the balance between sg stem cell self renewal and differentiation small molecule drug modulation of notch1 signaling to activate or inhibit the pathway enabled us to regulate sg differentiation to maintain skin oil levels providing a proof of principle that other signaling pathways downstream of krox20 could be therapeutic targets for sg related diseases authors yumeng zhang pernelle pulh michelle f pan yi he juanzhu yan annie li renée m mckay lu q le a rare tmem175 mutation drives parkinson s disease pathology by disrupting proton gating and lysosomal acidification xiaotong yang ping li man lv lingyong wang ruyi shan zikai jiang danzhen chen fangqian huang weijie cai liding zhao zuoyou guo xinhui chen zhidong cen yichang wang wei yang xinran li wei luo lin yang meiqin hu haoxing xu xiaotong yang ping li man lv lingyong wang ruyi shan zikai jiang danzhen chen fangqian huang weijie cai liding zhao zuoyou guo xinhui chen zhidong cen yichang wang wei yang xinran li wei luo lin yang meiqin hu haoxing xu view text pdf a rare tmem175 mutation drives parkinson s disease pathology by disrupting proton gating and lysosomal acidification text pdf abstract transmembrane protein 175 tmem175 implicated in parkinson s disease pd risk has been variably proposed to function as a background k leak channel or a proton activated proton channel in lysosomes here we identified the rare tmem175 variant p l275r in a patient with early onset pd electrophysiological analyses revealed that tmem175 l275r mutant proteins retain normal lysosomal expression and k leak activity but specifically lose proton and agonist dependent activation gating in skin fibroblasts isolated from the patient with pd harboring the monoallelic p l275r mutation tmem175 l275r and in derived induced pluripotent stem cells and induced dopaminergic neurons lysosomal h flux acidification and degradation were impaired these lysosomal defects were corrected upon genome editing to produce the isogenic wt allele cor but appeared when the mutant allele was introduced onto a wt background l275rmut pathological α synuclein aggregation was facilitated in patient derived l275r and mutation introduced l275rmut neurons consistent with these genetic findings pharmacological activation of tmem175 with small molecule agonists restored lysosomal functions and reduced α synuclein aggregation in tmem175 l275r neurons in in vivo studies equivalent site mutation knock in mice demonstrated synucleinopathy and pd like motor phenotypes collectively our work provides genetic and pharmacological evidence that severe loss of function mutations may contribute causally to the onset age and pathogenesis of pd and identifies lysosomal proton channels and transporters as potential therapeutic targets for pd intervention authors xiaotong yang ping li man lv lingyong wang ruyi shan zikai jiang danzhen chen fangqian huang weijie cai liding zhao zuoyou guo xinhui chen zhidong cen yichang wang wei yang xinran li wei luo lin yang meiqin hu haoxing xu enhancing treg persistence by inhibiting necroptosis restrains autoimmune pathology qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou view text pdf enhancing treg persistence by inhibiting necroptosis restrains autoimmune pathology text pdf abstract regulatory t cells tregs hold great promise as next generation therapeutics for autoimmune diseases however maintaining their functional persistence within inflamed tissues remains a major translational challenge using an in vitro system that recapitulates the inflammatory cns milieu of multiple sclerosis ms together with a pooled shrna screen we identify necroptotic signaling as a key driver of treg death thereby compromising treg functional persistence under inflammatory conditions we further demonstrate that tregs in both a mouse model of ms and patients with ms exhibited a preferential susceptibility to receptor interacting serine threonine kinase 1 dependent ripk1 dependent necroptosis mechanistically a foxp3 driven low glucose metabolic program rendered tregs intrinsically susceptible to necroptosis by limiting o glcnacylation o glcnac modification on ripk1 this vulnerability was not shared by conventional t cells under comparable inflammatory conditions finally in combination with adoptive treg transfer we show that selective inhibition of necroptosis in tregs enhanced their survival and suppressive function at sites of active inflammation thereby reducing autoimmune pathology in mouse models of ms and systemic lupus erythematosus together these findings identify necroptotic cell death as a barrier to treg persistence within inflamed tissues and highlight the therapeutic potential of necroptosis resistant tregs for the treatment of autoimmune diseases authors qiaoyan wu na cui li gao zhihui lu xiang ao rui pang xingyan li heling pan daichao xu peiying li junying yuan chengyu zou gene specific machine learning model epipred identifies likely pathogenic variants in the epilepsy related gene stxbp1 jeffrey d calhoun chengbing wang ca...
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