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1.
Open Forum Infect Dis ; 6(4): ofy290, 2019 Apr.
Article in English | MEDLINE | ID: mdl-31024967

ABSTRACT

BACKGROUND: Antimicrobial resistance is a major public health threat internationally but, particularly in India. A primary contributing factor to this rise in resistance includes unregulated access to antimicrobials. Implementing antimicrobial stewardship programs (ASPs) in the acute hospital setting will help curb inappropriate antibiotic use in India. Currently, ASPs are rare in India but are gaining momentum. This study describes ASP implementation in a large, academic, private, tertiary care center in India. METHODS: An ASP was established in February 2016 consisting of an administrative champion, hospitalist, microbiologist, intensivist, and pharmacists. Antimicrobial stewardship program interventions included postprescriptive audit and establishment of institutional guidelines. The ASP tracked appropriate drug selection including loading dose, maintenance dose, frequency, route, duration of therapy, de-escalation, and compliance with ASP recommendations. Defined daily dose (DDD) of drugs and cost of antimicrobials were compared between the pre-implementation phase (February 2015-January 2016) and post-implementation phase (February 2016-January 2017). RESULTS: Of 48 555 patients admitted during the post-implementation phase, 1020 received 1326 prescriptions for restricted antibiotics. Antibiotic therapy was appropriate in 56% (742) of the total patient prescriptions. A total of 2776 instances of "inappropriate" antimicrobial prescriptions were intervened upon by the ASP. Duration (806, 29%) was the most common reason for inappropriate therapy. Compliance with ASP recommendations was 54% (318). For all major restricted drugs, the DDD/1000 patient days declined, and there was a significant reduction in mean monthly cost by 14.4% in the post-implementation phase. CONCLUSIONS: Implementation of a multidisciplinary antibiotic stewardship program in this academic, large, Indian hospital demonstrated feasibility and economic benefits.

2.
Leukemia ; 24(11): 1920-6, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20882051

ABSTRACT

Survivin is an inhibitor of apoptosis protein family member that has an essential role in cellular proliferation as a component of the chromosome passenger complex. Survivin is highly expressed in embryos and in proliferating adult tissues, but it is not expressed in most differentiated cells. During tumorigenesis, however, survivin expression is dramatically upregulated. Although many studies have shown that survivin is required for cancer cells, the extent to which survivin contributes to the initiation of tumors is unknown. Here we show that transgenic mice that overexpress survivin in hematopoietic cells are at an increased risk of hematologic tumors. In examining how survivin might contribute to tumorigenesis, we observed that hematopoietic cells engineered to overexpress survivin are less susceptible to apoptosis. We conclude that survivin may promote tumorigenesis by imparting a survival advantage to cells that acquire additional genetic lesions.


Subject(s)
Hematologic Neoplasms/genetics , Microtubule-Associated Proteins/genetics , Up-Regulation , Animals , Apoptosis/genetics , Cell Differentiation , Cell Survival , Flow Cytometry , GATA1 Transcription Factor/genetics , Gene Expression Regulation, Neoplastic , Genetic Predisposition to Disease , Hematologic Neoplasms/pathology , Hematopoietic Stem Cells/physiology , Humans , Inhibitor of Apoptosis Proteins , Mice , Mice, Inbred BALB C , Neoplasm Proteins/genetics , Promoter Regions, Genetic , Spleen/immunology , Survivin , T-Lymphocytes/immunology
3.
Gene ; 399(2): 129-36, 2007 Sep 15.
Article in English | MEDLINE | ID: mdl-17574778

ABSTRACT

The role of vascular endothelial growth factor (VEGF) on cathepsin L expression was investigated in human glioblastoma cells (U87MG). Our results demonstrate the transcriptional upregulation of cathepsin L expression by VEGF. Transient transfection of U87MG cells with VEGF expression vector significantly increased cathepsin L activity. These results were further corroborated by a parallel increase in the mRNA levels and promoter activity of cathepsin L by VEGF. By deletion analysis, we identified a 47 base pair VEGF response element (VRE) in human cathepsin L promoter. Site directed mutagenesis studies demonstrated that both SP-1 and AP-4 motifs present in this region contribute to VEGF responsiveness. These results prove for the first time that over-expression of VEGF in human glioblastoma cells induces cathepsin L expression at the transcriptional level. This mechanism could be involved in the enhanced tumorogenic potential of these cells.


Subject(s)
Cathepsins/biosynthesis , Cysteine Endopeptidases/biosynthesis , Transcriptional Activation , Up-Regulation , Vascular Endothelial Growth Factor A/physiology , Base Sequence , Cathepsin L , Cathepsins/genetics , Cell Line, Tumor , Cysteine Endopeptidases/genetics , Gene Expression Regulation, Neoplastic , Glioblastoma , Humans , Molecular Sequence Data , Promoter Regions, Genetic , Response Elements
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