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Article ; Online: WD-repeat protein WDR13 is a novel transcriptional regulator of c-Jun and modulates intestinal homeostasis in mice.

Singh, Vijay Pratap / Katta, Saritha / Kumar, Satish

BMC cancer

2017 Volume 17, Issue 1, Page(s) 148

Abstract: Background: WDR13 is a member of the WD repeat protein family and is expressed in several tissues of human and mice. Previous studies in our laboratory showed that the lack of this gene in mice resulted in mild obesity, hyperinsulinemia, enhanced beta ... ...

Abstract	Background: WDR13 is a member of the WD repeat protein family and is expressed in several tissues of human and mice. Previous studies in our laboratory showed that the lack of this gene in mice resulted in mild obesity, hyperinsulinemia, enhanced beta cell proliferation and protection from inflammation. However, the molecular mechanism of WDR13 action is not well understood. Methods: In the present study, we used AOM/DSS to induce colitis-mediated colorectal tumor after establishing expression of Wdr13 gene in colon. Further, we have used human colon cancer cell lines, HT29 and COLO205, and mouse primary embryonic fibroblast to understand the molecular mechanism of WDR13 action. Results: We observed that mice lacking Wdr13 gene have reduced number of tumors and are more susceptible to DSS-induced colon ulcers. We also show that WDR13 is a part of multi protein complex c-Jun/NCoR1/HDAC3 and it acts as a transcriptional activator of AP1 target genes in the presence of JNK signal. Consistent with in vitro data, we observed reduced expression of AP1 target genes in colon after AOM/DSS treatment in Wdr13 knockout mice as compared to that in wild type. Conclusion: Mice lacking Wdr13 gene showed reduced expression of AP1 target genes and protection from colitis-induced colorectal tumors.
Language	English
Publishing date	2017-02-21
Publishing country	England
Document type	Journal Article
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-017-3118-7
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Article ; Online: Gender specific association of TP53 polymorphisms (EX4 215G>C Arg72Pro, IVS3+40-41ins16, and IVS6+62G>A), with risk of oral cancer subtypes and overall survival of the patients.

Nagam, Srivani L S S / Katta, Saritha / Prasad, Vidudala V T S

Molecular carcinogenesis

2017 Volume 56, Issue 3, Page(s) 895–912

Abstract: Reports on the association of TP53 polymorphisms with oral cancer are not only limited but also not specific to site and/or gender. Hence, we examined the effect of TP53 polymorphisms (EX4 215G>C, IVS3+40-41ins16 and IVS6+62G>A) on buccal mucosa cancer ( ... ...

Abstract	Reports on the association of TP53 polymorphisms with oral cancer are not only limited but also not specific to site and/or gender. Hence, we examined the effect of TP53 polymorphisms (EX4 215G>C, IVS3+40-41ins16 and IVS6+62G>A) on buccal mucosa cancer (BMC) and tongue cancer (TC) risk, survival of patients in relation to risk and clinical factors, gender wise (excepting for estimating hazards ratio [HR]), using Fisher's Exact Test, Kaplan-Meier analysis, and Cox-proportional hazards models. The exonic polymorphism increased BMC and TC risk in males by 2-4-fold. The IVS3+40-41ins16 was protective against BMC and TC in both genders, whereas IVS6+62G>A protected only males against TC. Genotype combinations and haplotypes which altered the risk of cancers in males and females were different. TC males, aged 40-44 years and females, aged 55-59 years survived better than BMC patients. The IVS3+40-41ins16 polymorphism differentially impacted survival of female patients exposed to tobacco. TC patients with EX4 215GC with lymphovascular spread (LVS) and metastasis exhibited higher HR while, patients with EX4 215CC and perineural invasion (PNI) showed lower HR. Impact of the intronic variants along with clinical parameters on survival and HR estimates varied between BMC and TC. Our bioinformatics analysis revealed the presence of CTCF binding site within TP53 gene. In conclusion, the polymorphisms altered risk and survival of BMC and TC in a gender specific manner, which varied with mode of tobacco and/or alcohol use. The current study, therefore underscores strong need for research, stratified by tumor site and gender. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Adult ; Binding Sites ; CCCTC-Binding Factor ; Computational Biology/methods ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Mouth Mucosa/pathology ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/pathology ; Neoplasm Metastasis ; Polymorphism, Genetic ; Repressor Proteins/metabolism ; Risk Factors ; Sex Factors ; Survival Analysis ; Tongue Neoplasms/genetics ; Tongue Neoplasms/metabolism ; Tongue Neoplasms/pathology ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	CCCTC-Binding Factor ; CTCF protein, human ; Repressor Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2017-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.22543
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Article ; Online: Susceptibility to oral cancers with CD95 and CD95L promoter SNPs may vary with the site and gender.

Daripally, Sarika / Nallapalle, Sateesh Reddy / Katta, Saritha / Prasad, Vidudala V T S

Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

2015 Volume 36, Issue 10, Page(s) 7817–7830

Abstract: We investigated risk association of oral cancers (tongue and buccal mucosa cancers) with FAS (-1377G > A and FAS -670 A > G) and FASL (-844 T > C) SNPs, in males and females. A case-control study of 535 oral cancer and 525 control subjects was performed. ...

Abstract	We investigated risk association of oral cancers (tongue and buccal mucosa cancers) with FAS (-1377G > A and FAS -670 A > G) and FASL (-844 T > C) SNPs, in males and females. A case-control study of 535 oral cancer and 525 control subjects was performed. SNPs were detected in the genomic DNA isolated from peripheral blood using PCR-RFLP. We report FASL -844 T > C SNPs increased risk for buccal mucosa cancer in females but not in males. On the other hand, FAS genotypes did not alter the risk of the cancers in both females and males. However, co-occurrence of FAS -1377 GA and -670 GG, FAS -1377 AA and -670 GG genotypes, and combined genotypes of FAS and FASL (FAS -1377 AA + FAS -670 GG + FASL -844 CC) alter male susceptibility towards tongue cancer. In females, combined genotypes of FAS (-1377GA and -670 AA) were found to be a risk factor of buccal mucosa cancer (OR = 3.27, CI = 1.28-8.36; P ≤ 0.01). FASL variants (GA and AA) increased tongue cancer risk in females who were tobacco users compared to non-tobacco users. In conclusion, SNPs of the FAS and FASL might alter risk of tongue and buccal mucosa cancers differentially, in a gender-dependent manner.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/mortality ; Carcinoma, Squamous Cell/secondary ; Carcinoma, Verrucous/genetics ; Carcinoma, Verrucous/mortality ; Carcinoma, Verrucous/secondary ; Case-Control Studies ; Fas Ligand Protein/genetics ; Female ; Follow-Up Studies ; Gender Identity ; Genetic Predisposition to Disease ; Genotype ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Mouth Mucosa ; Mouth Neoplasms/genetics ; Mouth Neoplasms/mortality ; Mouth Neoplasms/pathology ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/mortality ; Neoplasm Recurrence, Local/pathology ; Neoplasm Staging ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide/genetics ; Prognosis ; Promoter Regions, Genetic/genetics ; Risk Factors ; Survival Rate ; Young Adult ; fas Receptor/genetics
Chemical Substances	Fas Ligand Protein ; fas Receptor
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605825-5
ISSN	1423-0380 ; 0289-5447 ; 1010-4283
ISSN (online)	1423-0380
ISSN	0289-5447 ; 1010-4283
DOI	10.1007/s13277-015-3516-x
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Article ; Online: The molecular genetic basis of age-related macular degeneration: an overview.

Katta, Saritha / Kaur, Inderjeet / Chakrabarti, Subhabrata

Journal of genetics

2010 Volume 88, Issue 4, Page(s) 425–449

Abstract: Age-related macular degeneration (AMD) is a complex disorder of the eye and the third leading cause of blindness worldwide. With a multifactorial etiology, AMD results in progressive loss of central vision affecting the macular region of the eye in ... ...

Abstract	Age-related macular degeneration (AMD) is a complex disorder of the eye and the third leading cause of blindness worldwide. With a multifactorial etiology, AMD results in progressive loss of central vision affecting the macular region of the eye in elderly. While the prevalence is relatively higher in the Caucasian populations, it has gradually become a major public health issue among the non-Caucasian populations (including Indians) as well due to senescence, rapidly changing demographics and life-style factors. Recent genome-wide association studies (GWAS) on large case-control cohorts have helped in mapping genes in the complement cascade that are involved in the regulation of innate immunity with AMD susceptibility. Genes involved with mitochondrial oxidative stress and extracellular matrix regulation also play a role in AMD pathogenesis. Majority of the associations observed in complement (CFH, CFB, C2 and C3) and other (ARMS2 and HTRA1) genes have been replicated in diverse populations worldwide. Gene-gene (CFH with ARMS2 and HTRA1) interactions and correlations with environmental traits (smoking and body mass index) have been established as significant covariates in AMD pathology. In this review, we have provided an overview on the underlying molecular genetic mechanisms in AMD worldwide and highlight the AMD-associated-candidate genes and their potential role in disease pathogenesis.
MeSH term(s)	Chromosome Mapping ; Genetic Predisposition to Disease/genetics ; Genome, Human ; Genome-Wide Association Study ; Humans ; Lod Score ; Macular Degeneration/genetics ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2010-01-20
Publishing country	India
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3039-9
ISSN	0973-7731 ; 0958-8361 ; 0022-1333
ISSN (online)	0973-7731
ISSN	0958-8361 ; 0022-1333
DOI	10.1007/s12041-009-0064-4
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Article ; Online: Increased migration of antigen presenting cells to newly-formed lymphatic vessels in transplanted kidneys by glycol-split heparin.

Talsma, Ditmer T / Katta, Kirankumar / Boersema, Miriam / Adepu, Saritha / Naggi, Annamaria / Torri, Giangiacomo / Stegeman, Coen / Navis, Gerjan / van Goor, Harry / Hillebrands, Jan-Luuk / Yazdani, Saleh / van den Born, Jacob

PloS one

2017 Volume 12, Issue 6, Page(s) e0180206

Abstract: Background: Chronic renal transplant dysfunction is characterized by loss of renal function and tissue remodeling, including chronic inflammation and lymph vessel formation. Proteoglycans are known for their chemokine presenting capacity. We hypothesize ...

Abstract	Background: Chronic renal transplant dysfunction is characterized by loss of renal function and tissue remodeling, including chronic inflammation and lymph vessel formation. Proteoglycans are known for their chemokine presenting capacity. We hypothesize that interruption of the lymphatic chemokine-proteoglycan interaction interferes with the lymphatic outflow of leukocytes from the renal graft and might decrease the anti-graft allo-immune response. Methods: In a rat renal chronic transplant dysfunction model (female Dark-Agouti to male Wistar Furth), chemokines were profiled by qRT-PCR in microdissected tubulo-interstitial tissue. Disruption of lymphatic chemokine-proteoglycan interaction was studied by (non-anticoagulant) heparin-derived polysaccharides in vitro and in renal allografts. The renal allograft function was assessed by rise in plasma creatinine and urea. Results: Within newly-formed lymph vessels of transplanted kidneys, numerous CD45+ leukocytes were found, mainly MHCII+, ED-1-, IDO-, HIS14-, CD103- antigen presenting cells, most likely representing a subset of dendritic cells. Treatment of transplanted rats with regular heparin and two different (non-)anticoagulant heparin derivatives revealed worsening of kidney function only in the glycol-split heparin treated group despite a two-fold reduction of tubulo-interstitial leukocytes (p<0.02). Quantitative digital image analysis however revealed increased numbers of intra-lymphatic antigen-presenting cells only in the glycol-split heparin group (p<0.01). The number of intra-lymphatic leukocytes significantly correlates with plasma creatinine and urea, and inversely with creatinine clearance. Conclusions: Treatment of transplanted rats with glycol-split heparin significantly increases the number of intra-lymphatic antigen presenting cells, by increased renal diffusion of lymphatic chemokines, thereby increasing the activation and recruitment of antigen presenting cells towards the lymph vessel. This effect is unwanted in the transplantation setting, but might be advantageous in e.g., dendritic cell vaccination.
MeSH term(s)	Animals ; Antigen-Presenting Cells/cytology ; Cell Movement ; Enzyme-Linked Immunosorbent Assay ; Female ; Glycols/chemistry ; Heparin/chemistry ; Heparin/pharmacology ; Immunohistochemistry ; Kidney Transplantation ; Lymphatic Vessels/cytology ; Male ; Rats ; Rats, Wistar
Chemical Substances	Glycols ; Heparin (9005-49-6)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0180206
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Article ; Online: Increased migration of antigen presenting cells to newly-formed lymphatic vessels in transplanted kidneys by glycol-split heparin.

Ditmer T Talsma / Kirankumar Katta / Miriam Boersema / Saritha Adepu / Annamaria Naggi / Giangiacomo Torri / Coen Stegeman / Gerjan Navis / Harry van Goor / Jan-Luuk Hillebrands / Saleh Yazdani / Jacob van den Born

PLoS ONE, Vol 12, Iss 6, p e

2017 Volume 0180206

Abstract: Chronic renal transplant dysfunction is characterized by loss of renal function and tissue remodeling, including chronic inflammation and lymph vessel formation. Proteoglycans are known for their chemokine presenting capacity. We hypothesize that ... ...

Abstract	Chronic renal transplant dysfunction is characterized by loss of renal function and tissue remodeling, including chronic inflammation and lymph vessel formation. Proteoglycans are known for their chemokine presenting capacity. We hypothesize that interruption of the lymphatic chemokine-proteoglycan interaction interferes with the lymphatic outflow of leukocytes from the renal graft and might decrease the anti-graft allo-immune response.In a rat renal chronic transplant dysfunction model (female Dark-Agouti to male Wistar Furth), chemokines were profiled by qRT-PCR in microdissected tubulo-interstitial tissue. Disruption of lymphatic chemokine-proteoglycan interaction was studied by (non-anticoagulant) heparin-derived polysaccharides in vitro and in renal allografts. The renal allograft function was assessed by rise in plasma creatinine and urea.Within newly-formed lymph vessels of transplanted kidneys, numerous CD45+ leukocytes were found, mainly MHCII+, ED-1-, IDO-, HIS14-, CD103- antigen presenting cells, most likely representing a subset of dendritic cells. Treatment of transplanted rats with regular heparin and two different (non-)anticoagulant heparin derivatives revealed worsening of kidney function only in the glycol-split heparin treated group despite a two-fold reduction of tubulo-interstitial leukocytes (p<0.02). Quantitative digital image analysis however revealed increased numbers of intra-lymphatic antigen-presenting cells only in the glycol-split heparin group (p<0.01). The number of intra-lymphatic leukocytes significantly correlates with plasma creatinine and urea, and inversely with creatinine clearance.Treatment of transplanted rats with glycol-split heparin significantly increases the number of intra-lymphatic antigen presenting cells, by increased renal diffusion of lymphatic chemokines, thereby increasing the activation and recruitment of antigen presenting cells towards the lymph vessel. This effect is unwanted in the transplantation setting, but might be advantageous in e.g., dendritic cell vaccination.
Keywords	Medicine ; R ; Science ; Q
Subject code	630 ; 610
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: The involvement of complement factor B and complement component C2 in an Indian cohort with age-related macular degeneration.

Kaur, Inderjeet / Katta, Saritha / Reddy, Rajeev K / Narayanan, Raja / Mathai, Annie / Majji, Ajit B / Chakrabarti, Subhabrata

Investigative ophthalmology & visual science

2010 Volume 51, Issue 1, Page(s) 59–63

Abstract: Purpose: Genes involved in the complement cascade such as complement factor B (CFB) and complement component C2 have been implicated in age-related macular degeneration (AMD) worldwide. In continuation of the analysis of CFH and LOC387715/HTRA1, this ... ...

Abstract	Purpose: Genes involved in the complement cascade such as complement factor B (CFB) and complement component C2 have been implicated in age-related macular degeneration (AMD) worldwide. In continuation of the analysis of CFH and LOC387715/HTRA1, this study was conducted to gain understanding of the role of CFB and C2 in an Indian AMD cohort. Methods: Single nucleotide polymorphisms in CFB and C2 were screened in a cohort of clinically well-characterized patients with AMD (n = 177) and unaffected normal control subjects (n = 175). Screening was accomplished by a combination of customized genotyping followed by validation through resequencing. In addition, genotyping of two CFB variants (rs12614 and rs641153) that were in close proximity had to be resolved by resequencing. Estimates of allele and genotype frequencies, odds ratios, Hardy-Weinberg equilibrium, linkage disequilibrium (LD), and haplotype frequencies were also performed. Results: Three SNPs in C2 (rs547154 [IVS10]; P = 5.4 x 10(-11)) and CFB (rs641153 [R32Q], P = 2.2 x 10(-7) and rs2072633 [IVS17]; P = 2.0 x 10(-4)) were strongly associated with reduced risk of AMD. The rs547154 and rs641153 were in strong LD (D' = 0.90, 95% CI = 0.81-0.96) and a protective haplotype T-A was observed (OR = 0.10, 95% CI = 0.05-0.20). LD was moderate (D' = 0.77, 95% CI = 0.67-0.85) between the rs547154 and the rs2072633 SNPs, and the haplotype T-T generated with these SNPs was relatively less protective (OR = 0.28, 95% CI = 0.18-0.44). Conclusions: The results of the present study provide an independent validation of the association of rs547154 (C2) and rs641153 (CFB) SNPs with reduced risk of AMD in an Indian cohort.
MeSH term(s)	Alleles ; Asian Continental Ancestry Group/genetics ; Complement C2/genetics ; Complement Factor B/genetics ; Genotype ; Haplotypes ; Humans ; India ; Linkage Disequilibrium ; Macular Degeneration/genetics ; Odds Ratio ; Polymorphism, Single Nucleotide
Chemical Substances	Complement C2 ; Complement Factor B (EC 3.4.21.47)
Language	English
Publishing date	2010-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.09-4135
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Article ; Online: Renal heparan sulfate proteoglycans modulate fibroblast growth factor 2 signaling in experimental chronic transplant dysfunction.

Katta, Kirankumar / Boersema, Miriam / Adepu, Saritha / Rienstra, Heleen / Celie, Johanna W A M / Mencke, Rik / Molema, Grietje / van Goor, Harry / Berden, Jo H M / Navis, Gerjan / Hillebrands, Jan-Luuk / van den Born, Jacob

The American journal of pathology

2013 Volume 183, Issue 5, Page(s) 1571–1584

Abstract: Depending on the glycan structure, proteoglycans can act as coreceptors for growth factors. We hypothesized that proteoglycans and their growth factor ligands orchestrate tissue remodeling in chronic transplant dysfunction. We have previously shown ... ...

Abstract	Depending on the glycan structure, proteoglycans can act as coreceptors for growth factors. We hypothesized that proteoglycans and their growth factor ligands orchestrate tissue remodeling in chronic transplant dysfunction. We have previously shown perlecan to be selectively up-regulated in the glomeruli and arteries in a rat renal transplantation model. Using the same model, here we present quantitative RT-PCR profiling data on proteoglycans and growth factors from laser-microdissected glomeruli, arterial tunicae mediae, and neointimae at 12 weeks after transplantation. In glomeruli and neointimae of allografts, selective induction of the matrix heparan sulfate proteoglycan perlecan was observed, along with massive accumulation of fibroblast growth factor 2 (FGF2). Profiling the heparan sulfate polysaccharide side chains revealed conversion from a non-FGF2-binding heparan sulfate phenotype in control and isografted kidneys toward a FGF2-binding phenotype in allografts. In vitro experiments with perlecan-positive rat mesangial cells showed that FGF2-induced proliferation is dependent on sulfation and can be inhibited by exogenously added heparan sulfate. These findings indicate that matrix proteoglycans such as perlecan serve as functional docking platforms for FGF2 in chronic transplant dysfunction. We speculate that heparin-like glycomimetics could be a promising intervention to retard development of glomerulosclerosis and neointima formation in chronic transplant dysfunction.
MeSH term(s)	Allografts/metabolism ; Allografts/pathology ; Amino Acid Motifs ; Animals ; Cell Membrane/metabolism ; Cell Proliferation ; Chronic Disease ; Female ; Fibroblast Growth Factor 2/metabolism ; Heparan Sulfate Proteoglycans/metabolism ; Heparitin Sulfate/metabolism ; Kidney/metabolism ; Kidney/pathology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Transplantation/adverse effects ; Mesangial Cells/metabolism ; Mesangial Cells/pathology ; Protein Binding ; Proteoglycans/metabolism ; Rats ; Signal Transduction ; Up-Regulation
Chemical Substances	Heparan Sulfate Proteoglycans ; Proteoglycans ; Fibroblast Growth Factor 2 (103107-01-3) ; perlecan (143972-95-6) ; Heparitin Sulfate (9050-30-0)
Language	English
Publishing date	2013-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2013.07.030
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Article ; Online: Association of the del443ins54 at the ARMS2 locus in Indian and Australian cohorts with age-related macular degeneration.

Kaur, Inderjeet / Cantsilieris, Stuart / Katta, Saritha / Richardson, Andrea J / Schache, Maria / Pappuru, Rajeev R / Narayanan, Raja / Mathai, Annie / Majji, Ajit B / Tindill, Nicole / Guymer, Robyn H / Chakrabarti, Subhabrata / Baird, Paul N

Molecular vision

2013 Volume 19, Page(s) 822–828

Abstract: Purpose: The ARMS2/HTRA1 genes at the 10q26 locus have been associated with risk of age-related macular degeneration (AMD), with the most significantly associated variants being A69S (rs10490924), del443ins54 (EU427539) and rs11200638. We wished to ... ...

Abstract	Purpose: The ARMS2/HTRA1 genes at the 10q26 locus have been associated with risk of age-related macular degeneration (AMD), with the most significantly associated variants being A69S (rs10490924), del443ins54 (EU427539) and rs11200638. We wished to explore the association of the del443ins54 in two ethnically different populations from India and Australia. Methods: The del443ins54 was screened in a large cohort of ~1500 subjects from these two populations by a combination of PCR-based agarose gel electrophoresis and validated by resequencing. Statistical analysis comprised the calculations of allele, genotype and haplotype frequencies along with their p values and corresponding odds ratios (OR), and 95% confidence intervals (95% CI) and measures of linkage disequilibrium (LD). Results: The del443ins54 was significantly associated with AMD in both the Indian (p=1.74 × 10(-13); OR = 2.80, 95%CI, 2.12-3.70) and Australian cohorts (p = 2.78 × 10(-30); OR = 3.15, 95%CI, 2.58-3.86). These associations were similar to those previously identified for the A69S and the rs11200638 variant in these populations that also exhibited high degrees of LD (D' of 0.87-0.99). A major risk haplotype of "T-indel-A" (p = 5.7 × 10(-16); OR = 3.16, 95%CI, 2.34-4.19 and p=6.33 × 10(-30); OR = 3.15, 95%CI, 2.57-3.85) and a protective haplotype of "G-wild type-G" (p=2.35 × 10(-11); OR = 0.39, 95%CI, 0.29-0.52 and p=1.02 × 10(-30); OR = 0.31, 95%CI, 0.25-0.38) were identified in the Indian and Australian cohorts, respectively. Conclusions: These data provide an independent replication of the association of del443ins54 variant in two different ethnicities, despite differences in allele and haplotype frequencies between them. High levels of LD in both populations limit further genetic dissection of this region in AMD.
MeSH term(s)	Australia ; Cohort Studies ; Gene Frequency/genetics ; Genetic Association Studies ; Genetic Loci/genetics ; Genetic Predisposition to Disease ; Haplotypes/genetics ; High-Temperature Requirement A Serine Peptidase 1 ; Humans ; INDEL Mutation/genetics ; India ; Linkage Disequilibrium/genetics ; Macular Degeneration/genetics ; Polymorphism, Single Nucleotide/genetics ; Proteins/genetics ; Risk Factors ; Serine Endopeptidases/genetics
Chemical Substances	ARMS2 protein, human ; Proteins ; High-Temperature Requirement A Serine Peptidase 1 (EC 3.4.21.-) ; HTRA1 protein, human (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
Language	English
Publishing date	2013-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2017540-1
ISSN	1090-0535 ; 1090-0535
ISSN (online)	1090-0535
ISSN	1090-0535
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Article: Enantiomeric separation of Linezolid by chiral reversed-phase liquid chromatography.

Nirogi, Ramakrishna / Kota, Srinivasulu / Katta, Raja Rajeswari / Vennila, Saritha / Kandikere, Vishwottam / Mudigonda, Koteshwara / Vurimindi, Hima Bindu

Journal of chromatographic science

2008 Volume 46, Issue 9, Page(s) 764–766

Abstract: A chiral liquid chromatographic method is developed for the enantiomeric resolution of Linezolid, (S)(-)-N-[[-3-(3-fluoro-4-(4-morpholinyl)phenyl]-2-oxo-5-oxazolidinyl] methyl] acetamide, an antibiotic in bulk drugs. The enantiomers of Linezolid are ... ...

Abstract	A chiral liquid chromatographic method is developed for the enantiomeric resolution of Linezolid, (S)(-)-N-[[-3-(3-fluoro-4-(4-morpholinyl)phenyl]-2-oxo-5-oxazolidinyl] methyl] acetamide, an antibiotic in bulk drugs. The enantiomers of Linezolid are resolved on a Chiralcel OJ-RH column using a mobile phase system containing 150mM di-sodium hydrogen phosphate buffer (pH 4.5)-acetonitrile (86:14, v/v). The resolution between the enantiomers is found to be two. The developed method is extensively validated and proved to be robust. The limit of detection and limit of quantification of (R)-enantiomers are found to be 94 and 375 ng/mL, respectively, for 10 microL injection volume. The percentage recovery of (R)-enantiomer is ranged from 98.9 to 102.9 in bulk drug samples of Linezolid. Linezolid sample solution and mobile phase are found to be stable for at least 48 h. The proposed method is found to be suitable and accurate for the quantitative determination of (R)-enantiomer in bulk drugs.
MeSH term(s)	Acetamides/isolation & purification ; Chromatography, Liquid/methods ; Linezolid ; Oxazolidinones/isolation & purification ; Stereoisomerism
Chemical Substances	Acetamides ; Oxazolidinones ; Linezolid (ISQ9I6J12J)
Language	English
Publishing date	2008-11-12
Publishing country	United States
Document type	Journal Article ; Validation Studies
ZDB-ID	80141-0
ISSN	1945-239X ; 0021-9665
ISSN (online)	1945-239X
ISSN	0021-9665
DOI	10.1093/chromsci/46.9.764
Database	MEDical Literature Analysis and Retrieval System OnLINE

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