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1.
Jpn J Radiol ; 41(10): 1148-1156, 2023 Oct.
Article in English | MEDLINE | ID: mdl-37266825

ABSTRACT

PURPOSE: The aim of this study was to evaluate the utility of RAI therapy after reoperation for patients with LN relapse. MATERIALS AND METHODS: We retrospectively evaluated PTC patients who had undergone reoperation due to cervical LN recurrence. We used the chi-square test, Fisher's exact test, Student's t test and the Mann-Whitney U test to compare characteristics between patients retreated with RAI and those who did not receive RAI after reoperation. A multivariate logistic regression model was used to determine the association between RAI and biochemical response. By means of the Kaplan-Meier estimator and a multivariate Cox proportional hazard model, we assessed whether administration of RAI after reoperation is associated with improved prognosis. RESULTS: RAI therapy was closely associated with a superior biochemical response in all selected patients according to both univariate (p = 0.012) and multivariate analyses (p = 0.020). Thirteen of 97 patients developed a second recurrence or progression of structural disease during follow-up. A Kaplan-Meier progression-free survival (PFS) curve showed that high post-retreatment thyroglobulin (Tg) levels (≥ 1 ng/mL) were associated with unfavourable prognosis (p = 0.0172). In the subgroup analysis, univariate analysis revealed that only patients without extranodal invasion who received adjuvant RAI therapy achieved better PFS than those who did not receive RAI therapy (p = 0.0203). Multivariate analysis showed that RAI (p = 0.045) also improved PFS in patients without extranodal invasion. CONCLUSIONS: Adjuvant RAI after reoperation for PTC recurrence/persistence was associated with a favourable biochemical response and tended to increase PFS. Specifically, it was significantly associated with improved PFS only in patients without extranodal extension.


Subject(s)
Thyroid Neoplasms , Humans , Thyroid Cancer, Papillary/radiotherapy , Thyroid Cancer, Papillary/surgery , Thyroid Neoplasms/radiotherapy , Thyroid Neoplasms/surgery , Thyroid Neoplasms/pathology , Reoperation , Iodine Radioisotopes/therapeutic use , Retrospective Studies , Thyroidectomy , Neoplasm Recurrence, Local/radiotherapy , Lymph Nodes/pathology
2.
FEBS Lett ; 592(10): 1643-1666, 2018 05.
Article in English | MEDLINE | ID: mdl-29683472

ABSTRACT

Ganoderma is classified as a top grade traditional Chinese medicine for promoting human health by regulating 'vital energy'. Its potency towards metabolism and energy homeostasis, particularly, metabolic adaptations of adipocytes, needs to be re-evaluated through an evidence-based study. Here, the triterpenoid-rich Ganoderma tsugae ethanol extract (GTEE) was found to contribute towards adipogenesis accompanied with elevated intracellular lipid metabolic flux. Additionally, proteomic profiling revealed GTEE-upregulated mitochondrial remodeling and chemical energy redox modifications, which display UCP1-positive browning fat-selective features and a NADH-mediated adaptive mechanism. GTEE-treated mice with diet-induced obesity also resulted in the amelioration of white adipocyte hypertrophy and the appearance of UCP1-positive browning adipocytes. Our novel findings unravel that GTEE could promote intracellular metabolic flexibility and plasticity followed by the induction of adipocyte browning.


Subject(s)
Adipogenesis/drug effects , Drugs, Chinese Herbal/pharmacology , Fungal Proteins/metabolism , Ganoderma/metabolism , Proteomics , 3T3-L1 Cells , Adipocytes, Brown/metabolism , Adipocytes, White/metabolism , Animals , Blotting, Western , Diet , Drugs, Chinese Herbal/chemistry , Electrophoresis, Gel, Two-Dimensional , Ethanol/chemistry , Ganoderma/chemistry , Male , Mice , NAD/metabolism , Obesity/prevention & control , Organelle Biogenesis , Oxidation-Reduction , Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization , Uncoupling Protein 1/metabolism
3.
Food Funct ; 8(12): 4336-4346, 2017 Dec 13.
Article in English | MEDLINE | ID: mdl-28937704

ABSTRACT

Circulating levels of free fatty acids (FFAs) are often found to be increased in patients with type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS). High plasma FFA levels may give rise to maladaptive macrophage activation and promote inflammatory responses, which has been proposed as a potential mechanism for the development of DM and MS. P2X4 receptor (P2X4R), a ligand-gated cation channel activated by extracellular adenosine triphosphate (ATP), plays a primary role in the regulation of inflammatory responses. Puerarin has been reported to possess potential anti-inflammatory activity. However, the anti-inflammatory activity of puerarin and the underlying molecular mechanisms in a setting of a high concentration of FFAs remain unknown. In this study, we found that a high concentration of FFAs increased the expression of P2X4R, cytosolic Ca2+ concentration and the phosphorylation of extracellular signal-regulated kinase (ERK) and induced the expression of tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS) mRNA and the release of TNF-α and nitric oxide (NO) in RAW264.7 macrophages. Such a high concentration FFA-induced inflammation may be reversed by the P2X4R selective antagonist 5-BDBD, which manifests the important role of P2X4R in the TNF-α and NO release caused by the high concentration of FFAs in RAW264.7 cells. Molecular docking data showed that puerarin could interfere with the activation of P2X4R by forming hydrogen bonding towards residue Arg267, an important residue essential for the canonical activation of P2X4R. Treatment with puerarin dose-dependently reduced high concentration FFA-elevated P2X4R expression and inhibited P2X4R-mediated inflammatory signalling, including high concentration FFA-evoked [Ca2+]i, ERK phosphorylation, expression of TNF-α and iNOS mRNA and release of TNF-α and NO. Our findings emphasize the critical role of P2X4R in high concentration FFA-induced TNF-α and NO release of RAW264.7 macrophages. Puerarin notably counteracts these high concentration FFA-induced adverse effects through its inhibition of P2X4R expression and P2X4R-mediated inflammatory signalling.


Subject(s)
Diabetes Mellitus, Type 2/metabolism , Drugs, Chinese Herbal/pharmacology , Fatty Acids, Nonesterified/metabolism , Fatty Acids/adverse effects , Isoflavones/pharmacology , Nitric Oxide/metabolism , Protective Agents/pharmacology , Pueraria/chemistry , Receptors, Purinergic P2X4/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/genetics , Fatty Acids/metabolism , Humans , Macrophages/drug effects , Macrophages/metabolism , Mice , RAW 264.7 Cells , Receptors, Purinergic P2X4/genetics , Tumor Necrosis Factor-alpha/genetics
4.
Zhongguo Zhong Yao Za Zhi ; 41(15): 2883-2887, 2016 Aug.
Article in Chinese | MEDLINE | ID: mdl-28914033

ABSTRACT

To investigate the effect of turmeric volatile oil (TVO) on the apoptosis and proliferation of human skin SCC A431 cells, A431 cells were incubated with different concentrations (5-80 mg•L⁻¹) of TVO in vitro.The proliferation and cell cycle were assessed by CCK8 assay. The change of morphology was observed with inverted microscope. Apoptosis was evaluated with AO/EB double staining and flow cytometry (FCM); cell cycle was analyzed with FCM .Western blot method was used to detect caspase-3 and caspase-9 protein expression. Results indicated that TVO has significant inhibitory effects on the growth of A431 cells in a dose dependent relationship, the difference between groups has statistically significant (P<0.05). TVO group compared with control group, concentrations in cells shrivel and broken phenomenon, cell apoptosis rate increased, and a dose dependent and increased the expression of caspase-3 and caspase-9. The experiment results suggested that TVO could restrain skin squamous carcinoma A431 cells proliferation, and induce its apoptosis. The mechanism may be related to increase the expression of caspase-3 and caspase-9.


Subject(s)
Apoptosis , Curcuma/chemistry , Oils, Volatile/pharmacology , Skin/cytology , Caspase 3/metabolism , Caspase 9/metabolism , Cell Line, Tumor , Cell Proliferation , Humans
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