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Henan Tongwei Medical Equipment Co., LtdCall us : +86 − −19139704654 // Email us : [email protected]
The mechanistic basis for the biological properties of Morus alba flavonoid extract (MFE) and chemotherapy drug of doxorubicin on human colon cancer HT-29 cell line death are unknown The effect of doxorubicin and flavonoid extract on colon cancer HT-29 cell line death and identification of gene expression and PARP concentration of HT-29
Cardioprotective effects of curcumin and nebivolol against doxorubicin-induced cardiac toxicity in rats Show all authors S The protective effect of a purified extract of Withania somnifera against doxorubicin-induced cardiac toxicity Bawa-Khalfe T Identification of the molecular basis of doxorubicin-induced cardiotoxicity
However the molecular basis of the protective role of melatonin and the impact on doxorubicin response of breast cancer cells still largely remain to be elucidated This prompted us to perform a thorough analysis to decipher the functional role of melatonin on doxorubicin-treated breast cancer cells and to identify the molecular mechanisms and
Figure 1 EPCR cell surface total protein and mRNA levels in doxorubicin-treated HUVECs A cell surface levels of EPCR in doxorubicin (dox)–treated HUVECs were determined by flow cytometry using FITC-conjugated anti-EPCR (JRK 1535) monoclonal antibody B Western blot analysis of whole-cell EPCR levels in doxorubicin-treated HUVECs Lane 1 molecular
Interference with different mitochondrial processes is chief among the molecular and cellular determinants of doxorubicin cardiotoxicity contributing to the development of cardiomyopathy The present review provides the basis for the involvement of mitochondrial toxicity in the different functional hallmarks of anthracycline toxicity
Sleep is a highly conserved behavior critical to nervous system function Across species sleep amounts are highest in young animals and taper with maturity These ontogenetic changes to sleep have long been thought to facilitate brain maturation Indeed developmental sleep abnormalities are highly prevalent across neuropsychiatric disorders However knowledge of the genetic and molecular
Intravesical doxorubicin treatment delivers high drug concentrations to the bladder wall yet the treatment produces only a variable and incomplete response in superficial bladder cancer and insignificant activity in muscle-invading disease This study evaluated the pharmacological basis for the clinical observations and potential prognostic indicators of tumor sensitivity to doxorubicin
The underlying molecular mechanism of doxorubicin-induced HF is not completely consistent with non-pharmaceutical HF Some potential more important indicators specified for doxorubicin-induced HF may be concealed by the validation with the study GSE9128 designed for the identification
However the molecular basis of the protective role of melatonin and the impact on doxorubicin response of breast cancer cells still largely remain to be elucidated This prompted us to perform a thorough analysis to decipher the functional role of melatonin on doxorubicin-treated breast cancer cells and to identify the molecular
Nov 02 2012A team of scientists at the University of Texas MD Anderson Cancer Center have solved a longstanding mystery about doxorubicin's role in the destruction of heart tissue a finding that will help identify the patients who can safely tolerate the drug "Even in this age of targeted therapies doxorubicin
Thus Top2a is thought to be the molecular basis of doxorubicin's anti-tumor activity On the other hand doxorubicin is believed to cause dose-dependent cardiotoxicity through redox-cycling and generation of reactive oxygen species (ROS) Recently we showed that cardiomyocyte-specific deletion of Top2b protected cardiomyocytes from
title = Identification of the molecular basis of doxorubicin-induced cardiotoxicity abstract = Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS)
Jun 25 2016Zhang S Liu X Bawa-Khalfe T Lu L-S Lyu YL Liu LF Yeh ETH (2012) Identification of the molecular basis of doxorubicin-induced cardiotoxicity Nat Med 18(11):1639–1642 doi:10 1038/nm 2919 CAS Article PubMed Google Scholar
Breast cancer is a disease that is diverse in natural history response to treatment and patient outcomes It remains the most common non-cutaneous malignancy with an estimated 192 370 new cases in 2009 in the United States 1 Breast cancer-associated mortality is second only to lung cancer in the United States with an estimated 40 170 deaths in 2009 1 Breast cancer is also the most
In the present study we elucidate a molecular mechanism of AEG-1–induced chemoresistance an important characteristic of aggressive cancers AEG-1 increases the expression of multidrug resistance gene 1 (MDR1) protein resulting in increased efflux and decreased accumulation of doxorubicin promoting doxorubicin resistance
Doxorubicin is a highly effective anticancer agent but causes cardiotoxicity in many patients The mechanisms of doxorubicin-induced cardiotoxicity remain incompletely understood Here we investigated doxorubicin-induced cytotoxicity in human induced pluripotent stem cells-derived cardiomyocytes (iPS-CMs) We found that doxorubicin
Understanding the molecular mechanisms underlying multi-drug resistance (MDR) is one of the major challenges in current cancer research A phenomenon which is common to both intrinsic and acquired resistance is the aberrant alteration of gene expression in drug-resistant cancers
In an effort to reduce this limitation the incorporation of gene expression analyses has permitted the improvement in diagnosis prognosis prediction [23–25] and the identification of new molecular targets that may be used for the development of new drugs The new era of molecular
Identification of genes required for protection from doxorubicin by a genome-wide screen in Saccharomyces cerevisiae The basis for the antineoplastic effectiveness of anthracyclines (e g The identification of such a network of 40 genes strongly suggests the potential molecular pathways that confer doxorubicin
Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS) Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis
Doxorubicin hydrochloride liposome is a form of doxorubicin hydrochloride contained inside liposomes (very tiny particles of fat) This form may work better than other forms of doxorubicin hydrochloride and have fewer side effects Also because its effects last longer
The Genomics of Drug Sensitivity in Cancer Project is a collaboration between the Cancer Genome Project at the Wellcome Sanger Institute (UK) and the Center for Molecular Therapeutics Massachusetts General Hospital Cancer Center (USA) This work is funded by Wellcome
In the present study we elucidate a molecular mechanism of AEG-1–induced chemoresistance an important characteristic of aggressive cancers AEG-1 increases the expression of multidrug resistance gene 1 (MDR1) protein resulting in increased efflux and decreased accumulation of doxorubicin promoting doxorubicin
Molecular Basis of Doxorubicin-induced Cardiotoxicity Cardiology Grand Rounds Date: 2/27/13 1pm to 2pm Time: 2/27/13 1pm to 2pm Location: FCT3 5001 Format: Grand Rounds CME: 1 Hr Category 1 Speaker: Edward T H Yeh MD Speaker Bio: Professor and Chairman Department of Cardiology Division of Internal Medicine The University of Texas MD Anderson Cancer Center Houston TX
N2 - Doxorubicin an anthracycline antibiotic is a commonly used anticancer drug In spite of its widespread usage its therapeutic effect is limited by its cardiotoxicity On the cellular level Doxorubicin-induced cardiotoxicity manifests as stress induced premature senescence
A Prognostic Gene Expression Signature in the Molecular Classification of Chemotherapy-nave Urothelial Cancer is Predictive of Clinical Outcomes from Neoadjuvant Chemotherapy: A Phase 2 Trial of Dose-dense Methotrexate Vinblastine Doxorubicin
To explore the molecular basis of acquired resistance to bor-tezomib human monocytic/macrophage THP1 cells were exposed in vitro over a period of 6 months to stepwise increasing concentrations of bortezomib representing approximately 1- to 50-fold the IC 50 (2 5 nM to 200 nM)
Identification of the Molecular Basis of Doxorubicin-induced Cardiotoxicity Corresponding author: Edward T H Yeh Contents: Supplementary Figure 1a Top2b expression in the hearts by immunofluorescence Supplementary Figure 1b Top2b expression in the hearts by Western blot Supplementary Figure 2a Phospho-p53 expression in the hearts
Aug 01 2019In contrast to doxorubicin which displays a large volume of distribution (range 700 to 1100 L/m 2) the small steady state volume of distribution of liposomal doxorubicin suggests that Doxil is largely confined to vascular fluid Doxorubicin becomes available after the liposomes are extravasated
Treatment comprised rituximab 375 mg/m 2 cyclophosphamide 750 mg/m 2 doxorubicin 50 mg/m 2 all IV on day 1 and prednisone 100 mg/m 2 orally (PO) on days 1 to 5 plus either bortezomib 1 3 mg/m 2 IV on days 1 4 8 11 (VR-CAP) of each cycle or vincristine
Anthracycline-induced cardiotoxicity (ACT) is a key limiting factor in setting optimal chemotherapy regimes with almost half of patients expected to develop congestive heart failure given high doses However the genetic basis of sensitivity to anthracyclines remains unclear We created a panel of iPSC-derived cardiomyocytes from 45 individuals and performed RNA-seq after 24 hr exposure to
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