Polaron interfacial entropy as a route to high thermoelectric performance in DAE-doped PEDOT:PSS films.

Enhancing the thermoelectric transport properties of conductive polymer materials has been a long-term challenge, in spite of the success seen with molecular doping strategies. However, the strong coupling between the thermopower and the electrical conductivity limits thermoelectric performance. Here, we use polaron interfacial occupied entropy engineering to break through this intercoupling for a PEDOT:PSS (poly(3,4-ethylenedioxythiophene)-poly(4-styrenesulfonate)) thin film by using photochromic diarylethene (DAE) dopants coupled with UV-light modulation. With a 10-fold enhancement of the thermopower from 13.5 µV K-1 to 135.4 µV K-1 and almost unchanged electrical conductivity, the DAE-doped PEDOT:PSS thin film achieved an extremely high power factor of 521.28 µW m-1 K-2 from an original value of 6.78 µW m-1 K-2. The thermopower was positively correlated with the UV-light intensity but decreased with increasing temperature, indicating resonant coupling between the planar closed DAE molecule and PEDOT. Both the experiments and theoretical calculations consistently confirmed the formation of an interface state due to this resonant coupling. Interfacial entropy engineering of polarons could play a critical role in enhancing the thermoelectric performance of the organic film.

Ginsenoside Rg2 Attenuated Trastuzumab-Induced Cardiotoxicity in Rats.

AIM: Trastuzumab (TZM) is a monoclonal antibody drug for HER2-positive breast cancer by targeting epidermal growth factor 2, but it has significant cardiotoxicity. Ginsenoside Rg2 has shown a variety of biological activities. This study was aimed at investigating whether Rg2 attenuates TZM-induced cardiotoxicity. METHODS: A model of TZM-induced cardiotoxicity was established in Wistar rats, and the rats were pretreated with Rg2. After echocardiography analysis, the rats were killed and the hearts were dissected for RNAseq analysis. Primary human cardiomyocytes (HCMs) were treated with TZM with or without pretreatment with Rg2 and then subjected to a colony formation assay, flow cytometry analysis, and Western blot analysis for the detection of caspase-3, caspase-9, and BAX. RESULTS: TZM induced LV dysfunction in rats, but Rg2 could attenuate TZM-induced LV dysfunction. The mRNA levels of caspase-3, caspase-9, and BAX were significantly higher in TZM-treated rats. The colony formation ability of HCMs was significantly lower in TZM-treated cells but was recovered after pretreatment with Rg2. The apoptosis rate of HCMs was significantly higher in TZM-treated cells but was significantly lower after pretreatment with Rg2. Moreover, protein levels of caspase-3, caspase-9, and BAX were significantly higher in TZM-treated cells but were significantly lower after pretreatment with Rg2. CONCLUSION: Ginsenoside Rg2 inhibited TZM-induced cardiotoxicity, and the mechanism may be related to the downregulation of the expression of proapoptotic proteins caspase-3, caspase-9, and BAX and the inhibition of TZM-induced apoptosis in cardiomyocytes. Ginsenoside Rg2 has a potential to be applied in patients with breast cancer to prevent TZM-induced cardiotoxicity.

Ginsenoside Rg2 protects cardiomyocytes against trastuzumab-induced toxicity by inducing autophagy.

Trastuzumab (TZM) significantly improves the outcomes of patients with breast cancer; however, it is associated with severe cardiotoxicity. Ginsenoside Rg2 was reported to exert protective effects against myocardial injury and apoptosis in human cardiomyocytes (HCMs). However, whether ginsenoside Rg2 protects HCMs against TZM-induced toxicity remains unclear. The present study investigated the proliferation of HCMs using a Cell Counting Kit-8 assay and Ki67 immunofluorescence staining. Apoptotic cells were detected by Annexin V/propidium iodide staining and flow cytometry. Furthermore, monodansylcadaverine staining was performed to detect cell autophagy. In addition, western blotting was used to detect the expression levels of phosphorylated (p)-Akt, p-mTOR, beclin 1, microtubule associated protein 1 light chain 3α (LC3) and autophagy protein 5 (ATG5) in HCMs. Pretreatment with ginsenoside Rg2 significantly protected HCMs against TZM-induced cytotoxicity by inhibiting apoptosis. Furthermore, pretreatment with ginsenoside Rg2 induced autophagy in HCMs by upregulating the expression levels of p-Akt, p-mTOR, beclin 1, LC3 and ATG5. The results obtained in the present study suggested that ginsenoside Rg2 could protect HCMs against TZM-induced cardiotoxicity by activating autophagy. Therefore, ginsenoside Rg2 may serve as a potential therapeutic agent to prevent TZM-related cardiotoxicity in patients with breast cancer.

Dexrazoxane improves cardiac autonomic function in epirubicin-treated breast cancer patients with type 2 diabetes.

OBJECTIVE: The study objective was to investigate the protective effects of dexrazoxane (DRZ) on the cardiac autonomic nervous system (ANS) activity in anthracycline-treated breast cancer patients with diabetes. METHODS: A total of 110 early stage breast cancer patients with type 2 diabetes were divided randomly into 2 even groups: chemotherapy alone (Chemo) and chemotherapy + DRZ (Chemo + DRZ). All patients underwent adjuvant chemotherapy (80 mg/m epirubicin and 500 mg/m cyclophosphamide) for a total of 6 cycles with 21 days/cycle. The Chemo + DRZ group patients were treated intravenously with 800 mg/m DRZ 30 minutes prior to the administration of epirubicin, while the Chemo group patients were given saline. The cardiac ANS function was evaluated for each patient before and after 6 cycles of chemotherapy by resting heart rate (RHR) and heart rate variability (HRV), which was evaluated by both time and frequency domains. RESULTS: Before and after chemotherapy, patients in both groups showed significant decreases in HRV indices and increases in RHR and the low-frequency/high-frequency ratio. There were no significant differences between Chemo and Chemo + DRZ groups in terms of RHR and HRV indices before chemotherapy; however, after chemotherapy, patients in the Chemo group had a higher average RHR and lower HRV indices compared with patients in the Chemo + DRZ group. CONCLUSION: DRZ protects the cardiac ANS in epirubicin-treated early stage breast cancer patients with diabetes.

Dexrazoxane protects breast cancer patients with diabetes from chemotherapy-induced cardiotoxicity.

BACKGROUND: To evaluate the cardioprotective effect of dexrazoxane (DEX) on chemotherapy in patients with breast cancer with concurrent type 2 diabetes mellitus (DM2). METHODS: Eighty female patients with breast cancer with DM2 were randomly assigned to receive chemotherapy only or chemotherapy plus DEX. All patients received 80 mg/m epirubicin and 500 mg/m cyclophosphamide by intravenous infusion every 3 weeks for a total of 6 cycles. The group assigned to receive chemotherapy alone received placebo 30 minutes before epirubicin administration. The group assigned to receive chemotherapy plus DEX received 800 mg/m DEX 30 minutes before epirubicin administration. Cardiac function and hematology before and after 6 cycles of chemotherapy were analyzed. RESULTS: There was no difference in baseline systole or diastole function between the 2 DM2 groups. Patients receiving chemotherapy alone experienced significantly greater reductions in Ea and significantly greater elevations in E/Ea and Tei index in comparison with patients receiving chemotherapy plus DEX. After chemotherapy, superoxide dismutase was significantly reduced, and serum malondialdehyde (MDA) was significantly increased in patients with DM2. Serum superoxide dismutase levels were comparable between the 2 groups before and after chemotherapy, MDA levels were comparable between the 2 groups before chemotherapy, whereas serum MDA was significantly higher after chemotherapy in the chemotherapy alone group in comparison with the group that received DEX. CONCULSIONS: DEX protects against cardiotoxicity induced by chemotherapy in patients with breast cancer with concurrent DM2.