LIVIVO - Search results -

Search results

Result 1 - 10 of total 42

Search options

Article ; Online: An efficient Burrows-Wheeler transform-based aligner for short read mapping.

Guo, Lilu / Huo, Hongwei

Computational biology and chemistry

2024 Volume 110, Page(s) 108050

Abstract: ... based methods calculate on the compressed space. The source code is available: https://github.com/Lilu ... guo/Effaln. ...

Abstract	Read mapping as the foundation of computational biology is a bottleneck task under the pressure of sequencing throughput explodes. In this work, we present an efficient Burrows-Wheeler transform-based aligner for next-generation sequencing (NGS) short read. Firstly, we propose a difference-aware classification strategy to assign specific reads to the computationally more economical search modes, and present some acceleration techniques, such as a seed pruning method based on the property of maximum coverage interval to reduce the redundant locating for candidate regions, redesigning LF calculation to support fast query. Then, we propose a heuristic verification to determine the best mapping from amounts of flanking sequences. Incorporated with low-distortion string embedding, most dissimilar sequences are filtered out cheaply, and the highly similar sequences left are just right for the wavefront alignment algorithm's preference. We provide a full spectrum benchmark with different read lengths, the results show that our method is 1.3-1.4 times faster than state-of-the-art Burrows-Wheeler transform-based methods (including bowtie2, bwa-MEM, and hisat2) over 101bp reads and has a speedup with 1.5-13 times faster over 750bp to 1000bp reads; meanwhile, our method has comparable memory usage and accuracy. However, hash-based methods (including Strobealign, Minimap2, and Accel-Align) are significantly faster, in part because Burrows-Wheeler transform-based methods calculate on the compressed space. The source code is available: https://github.com/Lilu-guo/Effaln.
Language	English
Publishing date	2024-03-05
Publishing country	England
Document type	Journal Article
ISSN	1476-928X
ISSN (online)	1476-928X
DOI	10.1016/j.compbiolchem.2024.108050
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: MALAT1 accelerates proliferation and inflammation and suppresses apoptosis of endometrial stromal cells via the microRNA-142-3p/CXCR7 axis.

Tan, Kuailing / Mo, Hongying / Guo, Lilu / Wang, Binan

Reproductive biology

2022 Volume 22, Issue 3, Page(s) 100675

Abstract: MALAT1, microRNA (miR)-142-3p, and CXCR7 are critical molecules mediating endometriosis progression, and their correlation in endometriosis has been barely discussed. Thus, this research sought to survey the impact of MALAT1 on endometrial stromal cell ( ... ...

Abstract	MALAT1, microRNA (miR)-142-3p, and CXCR7 are critical molecules mediating endometriosis progression, and their correlation in endometriosis has been barely discussed. Thus, this research sought to survey the impact of MALAT1 on endometrial stromal cell (ESC) proliferation, apoptosis, and inflammation via miR-142-3p/CXCR7 axis to promote explorations on endometriosis. In endometrial tissues and ESCs, CXCR7 expression was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis and miR-142-3p and MALAT1 expression by qRT-PCR. Then, ESC proliferation was assessed by CCK-8 and EdU labeling assays, apoptosis by flow cytometry, and levels of inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in ESC supernatant by enzyme linked immunosorbent assay. The interactions among CXCR7, miR-142-3p, and MALAT1 were evaluated by dual luciferase reporter gene, RNA pull-down, and Argonaute 2- RNA immunoprecipitation assays. At last, the relevance of miR-142-3p to MALAT1 and that of miR-142-3p to CXCR7 in ectopic endometrial tissues were analyzed using Pearson correlation analysis. CXCR7 and MALAT1 were overexpressed whilst miR-142-3p was lowly expressed in ectopic endometrial tissues. CXCR7 silencing or miR-142-3p overexpression reduced proliferative ability and enhanced apoptosis rate in ESCs and decreased TNF-α, IL-1β, and IL-6 levels in cell supernatant. miR-142-3p negatively targeted CXCR7 while MALAT1 negatively targeted miR-142-3p. However, MALAT1 silencing diminished ESC proliferation and TNF-α, IL-1β, and IL-6 levels in ESC supernatant and elevated ESC apoptosis, which was counterweighed by inhibiting miR-142-3p. Conclusively, MALAT1 promoted ESC proliferation and inflammatory factor expression and inhibited ESC apoptosis via miR-142-3p/CXCR axis.
MeSH term(s)	Apoptosis ; Cell Proliferation ; Endometriosis/metabolism ; Endometriosis/pathology ; Female ; Humans ; Inflammation/metabolism ; Interleukin-6 ; MicroRNAs ; RNA, Long Noncoding/metabolism ; Stromal Cells ; Tumor Necrosis Factor-alpha
Chemical Substances	Interleukin-6 ; MALAT1 long non-coding RNA, human ; MIRN142 microRNA, human ; MicroRNAs ; RNA, Long Noncoding ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2022-07-25
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2189316-0
ISSN	2300-732X ; 1642-431X
ISSN (online)	2300-732X
ISSN	1642-431X
DOI	10.1016/j.repbio.2022.100675
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6095: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: MALAT1 accelerates proliferation and inflammation and suppresses apoptosis of endometrial stromal cells via the microRNA-142-3p/CXCR7 axis

Tan, Kuailing / Mo, Hongying / Guo, Lilu / Wang, Binan

Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn Reproductive Biology. 2022 Sept., v. 22, no. 3 p.100675-

2022

Abstract	MALAT1, microRNA (miR)-142-3p, and CXCR7 are critical molecules mediating endometriosis progression, and their correlation in endometriosis has been barely discussed. Thus, this research sought to survey the impact of MALAT1 on endometrial stromal cell (ESC) proliferation, apoptosis, and inflammation via miR-142-3p/CXCR7 axis to promote explorations on endometriosis. In endometrial tissues and ESCs, CXCR7 expression was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis and miR-142-3p and MALAT1 expression by qRT-PCR. Then, ESC proliferation was assessed by CCK-8 and EdU labeling assays, apoptosis by flow cytometry, and levels of inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in ESC supernatant by enzyme linked immunosorbent assay. The interactions among CXCR7, miR-142-3p, and MALAT1 were evaluated by dual luciferase reporter gene, RNA pull-down, and Argonaute 2- RNA immunoprecipitation assays. At last, the relevance of miR-142-3p to MALAT1 and that of miR-142-3p to CXCR7 in ectopic endometrial tissues were analyzed using Pearson correlation analysis. CXCR7 and MALAT1 were overexpressed whilst miR-142-3p was lowly expressed in ectopic endometrial tissues. CXCR7 silencing or miR-142-3p overexpression reduced proliferative ability and enhanced apoptosis rate in ESCs and decreased TNF-α, IL-1β, and IL-6 levels in cell supernatant. miR-142-3p negatively targeted CXCR7 while MALAT1 negatively targeted miR-142-3p. However, MALAT1 silencing diminished ESC proliferation and TNF-α, IL-1β, and IL-6 levels in ESC supernatant and elevated ESC apoptosis, which was counterweighed by inhibiting miR-142-3p. Conclusively, MALAT1 promoted ESC proliferation and inflammatory factor expression and inhibited ESC apoptosis via miR-142-3p/CXCR axis.
Keywords	Western blotting ; apoptosis ; endometriosis ; endometrium ; flow cytometry ; inflammation ; interleukin-6 ; luciferase ; microRNA ; precipitin tests ; reporter genes ; reverse transcriptase polymerase chain reaction ; tumor necrosis factors ; MALAT1 ; MicroRNA-142-3p ; CXCR7 ; Proliferation ; Endometrial stromal cells
Language	English
Dates of publication	2022-09
Publishing place	Elsevier B.V.
Document type	Article ; Online
ZDB-ID	2189316-0
ISSN	1642-431X
ISSN	1642-431X
DOI	10.1016/j.repbio.2022.100675
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Cologne/Königswinter

Zs.A 6095: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Osteonecrosis in Gaucher disease in the era of multiple therapies

Mohsen Basiri / Mohammad E Ghaffari / Jiapeng Ruan / Vagishwari Murugesan / Nathaniel Kleytman / Glenn Belinsky / Amir Akhavan / Andrew Lischuk / Lilu Guo / Katherine Klinger / Pramod K Mistry

eLife, Vol

Biomarker set for risk stratification from a tertiary referral center

2023 Volume 12

Abstract: Background: A salutary effect of treatments for Gaucher disease (GD) has been a reduction in the incidence of avascular osteonecrosis (AVN). However, there are reports of AVN in patients receiving enzyme replacement therapy (ERT) , and it is not known ... ...

Abstract	Background: A salutary effect of treatments for Gaucher disease (GD) has been a reduction in the incidence of avascular osteonecrosis (AVN). However, there are reports of AVN in patients receiving enzyme replacement therapy (ERT) , and it is not known whether it is related to individual treatments, GBA genotypes, phenotypes, biomarkers of residual disease activity, or anti-drug antibodies. Prompted by development of AVN in several patients receiving ERT, we aimed to delineate the determinants of AVN in patients receiving ERT or eliglustat substrate reduction therapy (SRT) during 20 years in a tertiary referral center. Methods: Longitudinal follow-ups of 155 GD patients between 2001 and 2021 were analyzed for episodes of AVN on therapy, type of therapy, GBA1 genotype, spleen status, biomarkers, and other disease indicators. We applied mixed-effects logistic model to delineate the independent correlates of AVN while receiving treatment. Results: The patients received cumulative 1382 years of treatment. There were 16 episodes of AVN in 14 patients, with two episodes, each occurring in two patients. Heteroallelic p.Asn409Ser GD1 patients were 10 times (95% CI, 1.5–67.2) more likely than p.Asn409Ser homozygous patients to develop osteonecrosis during treatment. History of AVN prior to treatment initiation was associated with 4.8-fold increased risk of AVN on treatment (95% CI, 1.5–15.2). The risk of AVN among patients receiving velaglucerase ERT was 4.68 times higher compared to patients receiving imiglucerase ERT (95% CI, 1.67–13). No patient receiving eliglustat SRT suffered AVN. There was a significant correlation between GlcSph levels and AVN. Together, these biomarkers reliably predicted risk of AVN during therapy (ROC AUC 0.894, p<0.001). Conclusions: There is a low, but significant risk of AVN in GD in the era of ERT/SRT. We found that increased risk of AVN was related to GBA genotype, history of AVN prior to treatment initiation, residual serum GlcSph level, and the type of ERT. No patient receiving SRT ...
Keywords	Gaucher disease ; avascular osteonecrosis ; lysosomal disease ; GBA1 ; glucosylsphingosine ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610 ; 616
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Osteonecrosis in Gaucher disease in the era of multiple therapies: Biomarker set for risk stratification from a tertiary referral center.

Basiri, Mohsen / Ghaffari, Mohammad E / Ruan, Jiapeng / Murugesan, Vagishwari / Kleytman, Nathaniel / Belinsky, Glenn / Akhavan, Amir / Lischuk, Andrew / Guo, Lilu / Klinger, Katherine / Mistry, Pramod K

eLife

2023 Volume 12

Abstract	Background: A salutary effect of treatments for Gaucher disease (GD) has been a reduction in the incidence of avascular osteonecrosis (AVN). However, there are reports of AVN in patients receiving enzyme replacement therapy (ERT) , and it is not known whether it is related to individual treatments, Methods: Longitudinal follow-ups of 155 GD patients between 2001 and 2021 were analyzed for episodes of AVN on therapy, type of therapy, Results: The patients received cumulative 1382 years of treatment. There were 16 episodes of AVN in 14 patients, with two episodes, each occurring in two patients. Heteroallelic p.Asn409Ser GD1 patients were 10 times (95% CI, 1.5-67.2) more likely than p.Asn409Ser homozygous patients to develop osteonecrosis during treatment. History of AVN prior to treatment initiation was associated with 4.8-fold increased risk of AVN on treatment (95% CI, 1.5-15.2). The risk of AVN among patients receiving velaglucerase ERT was 4.68 times higher compared to patients receiving imiglucerase ERT (95% CI, 1.67-13). No patient receiving eliglustat SRT suffered AVN. There was a significant correlation between GlcSph levels and AVN. Together, these biomarkers reliably predicted risk of AVN during therapy (ROC AUC 0.894, p<0.001). Conclusions: There is a low, but significant risk of AVN in GD in the era of ERT/SRT. We found that increased risk of AVN was related to Funding: LSD Training Fellowship from Sanofi to MB.
MeSH term(s)	Humans ; Gaucher Disease/complications ; Gaucher Disease/drug therapy ; Gaucher Disease/genetics ; Tertiary Care Centers ; Biomarkers/metabolism ; Osteonecrosis/complications ; Osteonecrosis/epidemiology ; Risk Assessment
Chemical Substances	sphingosyl beta-glucoside (52050-17-6) ; Biomarkers
Language	English
Publishing date	2023-05-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.87537
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Lipid peroxidation generates biologically active phospholipids including oxidatively N-modified phospholipids.

Davies, Sean S / Guo, Lilu

Chemistry and physics of lipids

2014 Volume 181, Page(s) 1–33

Abstract: Peroxidation of membranes and lipoproteins converts "inert" phospholipids into a plethora of oxidatively modified phospholipids (oxPL) that can act as signaling molecules. In this review, we will discuss four major classes of oxPL: mildly oxygenated ... ...

Abstract	Peroxidation of membranes and lipoproteins converts "inert" phospholipids into a plethora of oxidatively modified phospholipids (oxPL) that can act as signaling molecules. In this review, we will discuss four major classes of oxPL: mildly oxygenated phospholipids, phospholipids with oxidatively truncated acyl chains, phospholipids with cyclized acyl chains, and phospholipids that have been oxidatively N-modified on their headgroups by reactive lipid species. For each class of oxPL we will review the chemical mechanisms of their formation, the evidence for their formation in biological samples, the biological activities and signaling pathways associated with them, and the catabolic pathways for their elimination. We will end by briefly highlighting some of the critical questions that remain about the role of oxPL in physiology and disease.
MeSH term(s)	Animals ; Humans ; Lipid Peroxidation ; Phospholipids/chemistry ; Phospholipids/metabolism ; Signal Transduction
Chemical Substances	Phospholipids
Language	English
Publishing date	2014-04-02
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	213869-4
ISSN	1873-2941 ; 0009-3084
ISSN (online)	1873-2941
ISSN	0009-3084
DOI	10.1016/j.chemphyslip.2014.03.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 804: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Incremental biomarker and clinical outcomes after switch from enzyme therapy to eliglustat substrate reduction therapy in Gaucher disease.

Kleytman, Nathaniel / Ruan, Jiapeng / Ruan, Audrey / Zhang, Bailin / Murugesan, Vagishwari / Lin, Haiqun / Guo, Lilu / Klinger, Katherine / Mistry, Pramod K

Molecular genetics and metabolism reports

2021 Volume 29, Page(s) 100798

Abstract: In Gaucher disease (GD), genetic deficiency of acid β-glucosidase leads to accumulation of its substrate glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph). Lipid-laden cells, most prominently seen as macrophages engorged with GlcCer and GlcSph- ... ...

Abstract	In Gaucher disease (GD), genetic deficiency of acid β-glucosidase leads to accumulation of its substrate glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph). Lipid-laden cells, most prominently seen as macrophages engorged with GlcCer and GlcSph-laden lysosomes, trigger chronic metabolic inflammation and multisystemic phenotypes. Among the pleiotropic effects of inflammatory cascades, the induction of glucosylceramide synthase accentuates the primary metabolic defect. First-line therapies for adults with GD type 1 include Enzyme Replacement Therapy (ERT) and eliglustat Substrate Reduction Therapy (SRT). The ENCORE phase 3 clinical trial of eliglustat demonstrated non-inferiority compared to ERT. It is not known whether switching stable patients from long-term ERT to SRT results in the incremental reversal of the disease phenotype and its surrogate indicators. Herein, we report real-world experience from a single tertiary referral center of 38 adult GD type 1 patients, stable on long-term ERT (mean 13.3 years), who switched to eliglustat SRT (mean 3.1 years). After switch to SRT, there was significant reduction in spleen volume (
Language	English
Publishing date	2021-08-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2021.100798
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Incremental biomarker and clinical outcomes after switch from enzyme therapy to eliglustat substrate reduction therapy in Gaucher disease

Nathaniel Kleytman / Jiapeng Ruan / Audrey Ruan / Bailin Zhang / Vagishwari Murugesan / Haiqun Lin / Lilu Guo / Katherine Klinger / Pramod K. Mistry

Molecular Genetics and Metabolism Reports, Vol 29, Iss , Pp 100798- (2021)

2021

Abstract	In Gaucher disease (GD), genetic deficiency of acid β-glucosidase leads to accumulation of its substrate glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph). Lipid-laden cells, most prominently seen as macrophages engorged with GlcCer and GlcSph-laden lysosomes, trigger chronic metabolic inflammation and multisystemic phenotypes. Among the pleiotropic effects of inflammatory cascades, the induction of glucosylceramide synthase accentuates the primary metabolic defect. First-line therapies for adults with GD type 1 include Enzyme Replacement Therapy (ERT) and eliglustat Substrate Reduction Therapy (SRT). The ENCORE phase 3 clinical trial of eliglustat demonstrated non-inferiority compared to ERT. It is not known whether switching stable patients from long-term ERT to SRT results in the incremental reversal of the disease phenotype and its surrogate indicators. Herein, we report real-world experience from a single tertiary referral center of 38 adult GD type 1 patients, stable on long-term ERT (mean 13.3 years), who switched to eliglustat SRT (mean 3.1 years). After switch to SRT, there was significant reduction in spleen volume (P = 0.003) while liver volume, which was normal at baseline, remained unchanged. Platelet counts increased significantly (P = 0.026). Concomitantly, there was reduction of three validated biomarkers of Gaucher disease activity: plasma GlcSph decreased from 63.7 ng/ml (95% CI, 37.6-89.8) to 26.1 ng/ml (95% CI, 15.7-36.6) (P < 0.0001); chitotriosidase fell from 1136.6 nmol/ml/h (95% CI, 144.7-2128.6) to 466.9 nmol/ml/h (95% CI, 209.9-723.9) (P = 0.002); and glycoprotein non-metastatic melanoma B (gpNMB) decreased from 59.3 ng/ml (95% CI, 39.7-78.9) to 43.6 ng/ml (95% CI, 30.7-56.6) (P = 0.0006). There were no episodes of avascular necrosis or fractures in patients on SRT. Patients reported favorable experiences of switching from alternate week infusions to oral therapy. Collectively, these results demonstrate that the switch to eliglustat SRT from ERT leads to incremental ...
Keywords	Gaucher disease ; Substrate reduction therapy ; Glucosylsphingosphingosine ; Eliglustat ; Splenomegaly ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Bioactive aldehyde-modified phosphatidylethanolamines.

Guo, Lilu / Davies, Sean S

Biochimie

2013 Volume 95, Issue 1, Page(s) 74–78

Abstract: Lipid peroxidation generates a variety of lipid aldehydes, which have been recognized to modify protein and DNA, causing inflammation and cancer. However, recent studies demonstrate that phosphatidylethanolamine (PE) is a major target for these aldehydes, ...

Abstract	Lipid peroxidation generates a variety of lipid aldehydes, which have been recognized to modify protein and DNA, causing inflammation and cancer. However, recent studies demonstrate that phosphatidylethanolamine (PE) is a major target for these aldehydes, forming aldehyde-modified PEs (al-PEs) as a novel family of mediators for inflammation. This review summarizes our current understanding of these al-PEs, including formation, detection, structural characterization, physiological relevance and mechanism of action.
MeSH term(s)	Aldehydes/chemistry ; Aldehydes/metabolism ; Endoplasmic Reticulum/chemistry ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress/physiology ; Humans ; Lipid Peroxidation ; Molecular Structure ; Oxidative Stress ; Phosphatidylethanolamines/chemistry ; Phosphatidylethanolamines/metabolism ; Reactive Oxygen Species/chemistry ; Reactive Oxygen Species/metabolism
Chemical Substances	Aldehydes ; Phosphatidylethanolamines ; Reactive Oxygen Species
Language	English
Publishing date	2013-01
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2012.07.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.135: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Neuroinflammation in neuronopathic Gaucher disease: Role of microglia and NK cells, biomarkers, and response to substrate reduction therapy.

Boddupalli, Chandra Sekhar / Nair, Shiny / Belinsky, Glenn / Gans, Joseph / Teeple, Erin / Nguyen, Tri-Hung / Mehta, Sameet / Guo, Lilu / Kramer, Martin L / Ruan, Jiapeng / Wang, Honggge / Davison, Matthew / Kumar, Dinesh / Vidyadhara, D J / Zhang, Bailin / Klinger, Katherine / Mistry, Pramod K

eLife

2022 Volume 11

Abstract: Background: Neuronopathic Gaucher disease (nGD) is a rare neurodegenerative disorder caused by biallelic mutations in : Methods: Here, using single-cell resolution of mouse nGD brains, lipidomics, and newly generated biomarkers, we found induction of ...

Abstract	Background: Neuronopathic Gaucher disease (nGD) is a rare neurodegenerative disorder caused by biallelic mutations in Methods: Here, using single-cell resolution of mouse nGD brains, lipidomics, and newly generated biomarkers, we found induction of neuroinflammation pathways involving microglia, NK cells, astrocytes, and neurons. Results: Targeted rescue of Conclusions: Together, our study delineates individual cellular effects of Funding: Research grant from Sanofi; other support includes R01NS110354, Yale Liver Center P30DK034989, pilot project grant.
MeSH term(s)	Animals ; Biomarkers ; Gaucher Disease/drug therapy ; Glucosylceramidase/genetics ; Glucosylceramidase/metabolism ; Glycosphingolipids ; Killer Cells, Natural/metabolism ; Mice ; Microglia/metabolism ; Neuroinflammatory Diseases ; Pilot Projects
Chemical Substances	Biomarkers ; Glycosphingolipids ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2022-08-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.79830
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito