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1.
Clin Transl Oncol ; 23(1): 155-163, 2021 Jan.
Article in English | MEDLINE | ID: mdl-32488804

ABSTRACT

PURPOSE: To analyze the correlation between contrast-enhanced ultrasound image features and axillary lymph node metastasis of primary breast cancer and its diagnostic value. METHODS: In this study, 64 patients with axillary lymph node metastasis of primary breast cancer diagnosed and treated in our hospital from February 2011 to March 2013 were collected as an observation group, and 54 patients without axillary lymph node metastasis were collected as a control group. All patients underwent a contrast-enhanced ultrasound examination, and the correlation between the contrast-enhanced ultrasound image features and axillary lymph node metastasis and its diagnostic value were analyzed. They were divided into two groups according to their survival conditions: the group with good efficacy and group with poor efficacy, and the prognostic factors of breast cancer in the two groups were analyzed. RESULTS: There were statistical differences in the peripheral acoustic halo, blood flow classification, ratio of length to diameter (L/D), maximum cortical thickness, and enhancement mode of lymph nodes between the two groups (p < 0.05). The area under ROC curve for diagnosis of axillary lymph node metastasis by contrast-enhanced ultrasound was 0.854, sensitivity was 83.33%, and specificity was 87.5%; L/D and enhancement mode were independent prognostic factors for breast cancer. CONCLUSIONS: Contrast-enhanced ultrasound image features have diagnostic and prognostic value for axillary lymph node metastasis of breast cancer.


Subject(s)
Breast Neoplasms/diagnostic imaging , Contrast Media , Lymph Nodes/diagnostic imaging , Lymphatic Metastasis/diagnostic imaging , Analysis of Variance , Axilla , Breast Neoplasms/mortality , Breast Neoplasms/pathology , Breast Neoplasms/physiopathology , Case-Control Studies , Female , Humans , Lymph Nodes/pathology , Lymphatic Metastasis/pathology , Middle Aged , Outcome Assessment, Health Care , ROC Curve , Regional Blood Flow , Regression Analysis , Sensitivity and Specificity
2.
Genet Mol Res ; 16(2)2017 May 10.
Article in English | MEDLINE | ID: mdl-28510254

ABSTRACT

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects motor neurons and lacks an effective treatment. The disease pathogenesis has not been clarified at present. Pathological transactive response DNA-binding protein 43 (TDP-43) plays an important role in the pathogenesis of ALS. Nuclear translocation of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is found in a mutant TDP-43 transgenic cell model, but its downstream antioxidant enzyme expression is decreased. To elucidate the specific mechanism of Nrf2/ARE (antioxidant responsive element) signaling dysfunction, we constructed an ALS cell model with human mutant TDP-43 using the NSC-34 cell line to evaluate the impact of the TDP-43 mutation on the Nrf2/ARE pathway. We found the nuclear translocation of Nrf2, but the expression of total Nrf2, cytoplasmic Nrf2, and downstream phase II detoxifying enzyme (NQO1) was decreased in NSC-34 cells transfected with the TDP-43-M337V plasmid. Besides, TDP-43-M337V plasmid-transfected NSC-34 cells were rounded with reduced neurites, shortened axons, increased levels of intracellular lipid peroxidation products, and decreased viability, which suggests that the TDP-43-M337V plasmid weakened the antioxidant capacity of NSC-34 cells and increased their susceptibility to oxidative damage. We further showed that expression of the MafK protein and the Jun dimerization protein 2 (JDP2) was reduced in TDP-43-M337V plasmid-transfected NSC-34 cells, which might cause accumulation of Nrf2 in nuclei but a decrease in NQO1 expression. Taken together, our results confirmed that TDP-43-M337V impaired the Nrf2/ARE pathway by reducing the expression of MafK and JDP2 proteins, and provided information for further research on the molecular mechanisms of TDP-43-M337V in ALS.


Subject(s)
Amyotrophic Lateral Sclerosis/metabolism , DNA-Binding Proteins/metabolism , MafK Transcription Factor/metabolism , Mutation, Missense , NF-E2-Related Factor 2/metabolism , Repressor Proteins/metabolism , Response Elements , Animals , Cell Line , DNA-Binding Proteins/genetics , MafK Transcription Factor/genetics , Mice , NAD(P)H Dehydrogenase (Quinone)/metabolism , Neurons/metabolism , Oxidative Stress , Repressor Proteins/genetics
3.
West Indian Med J ; 64(3): 195-200, 2015 Jun.
Article in English | MEDLINE | ID: mdl-26426169

ABSTRACT

OBJECTIVE: To examine the effect of the alcoholic extract of lotus leaves (AELL) on antiretroviral treatment-induced dyslipidaemia in a rat model. METHODS: Lotus leaves were extracted by 95% ethanol. Seventy male Sprague-Dawley rats were given lopinavir/ritonavir for six weeks. At week 0 and 6, sera were collected for measurement of total cholesterol (TC) and triglyceride (TG). Rats meeting the criteria for dyslipidaemia were assigned to four groups and received once daily for another four weeks lopinavir/ritonavir (group A), lopinavir/ritonavir plus 0.52 g/kg AELL (group B), lopinavir/ritonavir plus 0.26 g/kg AELL (group C), or lopinavir/ritonavir plus 0.13 g/kg AELL (group D), respectively. At weeks 8 and 10, blood samples were collected again for measurement of TC or TG. RESULTS: Both TC and TG increased over time in group A during the observation period (weeks 6 to 10), however, TC and TG decreased in group B, and TG declined in group C. Neither TC nor TG could be reduced to a level near baseline. CONCLUSION: Alcoholic extract of lotus leaves may have the potential to treat dyslipidaemia related to highly active antiretroviral therapy, but may not be potent enough to reduce TC or TG concentrations to goal levels when used alone.

4.
Braz J Med Biol Res ; 43(3): 271-8, 2010 Mar.
Article in English | MEDLINE | ID: mdl-20401435

ABSTRACT

Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer MGC803 cells. In this study, 15 mg/L DADS exerted similar effects on growth and cell cycle arrest in human gastric cancer BGC823 cells. Due to the importance of cell cycle redistribution in DADS-mediated anti-carcinogenic effects, we investigated the role of checkpoint kinases (Chk1 and Chk2) during DADS-induced cell cycle arrest. We hypothesized that DADS could mediate G2/M phase arrest through either Chk1 or Chk2 signal transduction pathways. We demonstrated that DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, and that DADS down-regulated Cdc25C and cyclin B1. The expression of mRNA and total protein for Chkl and Chk2 was unchanged. Chk1 is specifically phosphorylated by ATR (ATM-RAD3-related gene). Western blot analysis showed that phospho-ATR was activated by DADS. Taken together, these data suggest that cell cycle G2/M arrest, which was associated with accumulation of the phosphorylated forms of Chk1, but not of Chk2, was involved in the growth inhibition induced by DADS in the human gastric cancer cell line BGC823. Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.


Subject(s)
Allyl Compounds/pharmacology , Antineoplastic Agents/pharmacology , Disulfides/pharmacology , G2 Phase/drug effects , Growth Inhibitors/pharmacology , Protein Kinases/drug effects , Stomach Neoplasms/enzymology , Cell Division/drug effects , Cell Line, Tumor , Checkpoint Kinase 1 , Humans , Protein Kinases/metabolism , Signal Transduction/drug effects , Stomach Neoplasms/pathology
5.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;43(3): 271-278, Mar. 2010. ilus, tab, graf
Article in English | LILACS | ID: lil-539713

ABSTRACT

Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer MGC803 cells. In this study, 15 mg/L DADS exerted similar effects on growth and cell cycle arrest in human gastric cancer BGC823 cells. Due to the importance of cell cycle redistribution in DADS-mediated anti-carcinogenic effects, we investigated the role of checkpoint kinases (Chk1 and Chk2) during DADS-induced cell cycle arrest. We hypothesized that DADS could mediate G2/M phase arrest through either Chk1 or Chk2 signal transduction pathways. We demonstrated that DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, and that DADS down-regulated Cdc25C and cyclin B1. The expression of mRNA and total protein for Chkl and Chk2 was unchanged. Chk1 is specifically phosphorylated by ATR (ATM-RAD3-related gene). Western blot analysis showed that phospho-ATR was activated by DADS. Taken together, these data suggest that cell cycle G2/M arrest, which was associated with accumulation of the phosphorylated forms of Chk1, but not of Chk2, was involved in the growth inhibition induced by DADS in the human gastric cancer cell line BGC823. Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.


Subject(s)
Humans , Allyl Compounds/pharmacology , Antineoplastic Agents/pharmacology , Disulfides/pharmacology , /drug effects , Growth Inhibitors/pharmacology , Protein Kinases/drug effects , Stomach Neoplasms/enzymology , Cell Line, Tumor , Cell Division/drug effects , Protein Kinases/metabolism , Signal Transduction/drug effects , Stomach Neoplasms/pathology
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