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No practical predictive biomarkers exist to date for the response to androgen receptor-axis targeted (ARAT) therapies in metastatic castration-resistant prostate cancer (mCRPC). This study investigated whether prostate-specific antigen (PSA) kinetics in primary androgen-deprivation therapy for advanced hormone-sensitive prostate cancer may be associated with the response to ARAT agents in mCRPC.This study assessed 102 patients with mCRPC treated with enzalutamide or abiraterone to evaluate the associations between clinical outcomes and PSA kinetics, including the ratio of initial to nadir PSA (I/N PSA) level in primary combined androgen blockade. The PSA response was defined as a ≥50% decrease at 3 months from baseline in patients with mCRPC.In patients treated with enzalutamide, the optimal cut-off I/N PSA value for PSA response was 531 ng/ml (sensitivity=66.7%, specificity=88.2%, area under the curve=0.73, using a receiver operating characteristic curve). The PSA response was 83.3% and 25.0% in the high and low I/N PSA groups, respectively. The median overall survival and radiographic progression-free survival from enzalutamide initiation were longer for the high compared to the low I/N PSA group. Multivariate analysis revealed I/N PSA (hazard ratio=0.275, p=0.026) as an independent risk factor for overall survival in the patients treated with enzalutamide. In contrast, I/N PSA showed no predictive ability for PSA response in patients treated with abiraterone.In patients with mCRPC, I/N PSA can be a practical predictive biomarker for response to the ARAT agent enzalutamide.

We aimed to clarify the association between body mass index (BMI) and clinical outcomes of pembrolizumab treatment for advanced urothelial cancer (UC).We retrospectively reviewed the records of patients with advanced UC who received pembrolizumab after chemotherapy between March 2018 and December 2021. Patients were divided according to BMI into the non-overweight group (BMI25 kg/mOf 84 eligible patients, 63 (75%) and 21 (25%) were in the non-overweight and overweight groups, respectively. Although the objective response rate was higher in the overweight group (55%) than that in the non-overweight group (29%), the difference was not significant. Progression-free survival (PFS) was significantly longer in the overweight group (median 15.2 months) than that in the non-overweight group (median 4.8 months; p=0.01). Overall survival was also longer in the overweight group (median 36.1 months) compared to that in the non-overweight group (13.4 months), but the difference was not significant (p=0.11). Multivariable analysis showed that overweight was significantly associated with favourable PFS. Any and severe (grade 3) irAEs were observed in 15 (24%) and 5 (7.9%) patients in the non-overweight group, respectively, and in 8 (38%) and 2 (9.5%) patients in the overweight group, respectively, but the differences were not significant.BMI was associated with oncological outcomes in patients with advanced UC who received pembrolizumab but not with the development of irAEs.

Although the sequential use of abiraterone and enzalutamide is not recommended because of possible cross-resistance, many patients with metastatic castration-resistant prostate cancer (mCRPC) are receiving sequential abiraterone and enzalutamide in the real world, and a subset of patients can benefit from sequential therapy with these drugs. This study aimed to identify patients who could benefit from the sequential use of enzalutamide after abiraterone use.We included 70 patients with mCRPC who received enzalutamide sequentially following abiraterone treatment. Decline in the prostatespecific antigen (PSA) levels at 4 weeks after enzalutamide initiation and the association between decline in PSA levels and survival were analyzed.Sixteen men (22.9%) achieved a decline of50% in PSA levels after 4 weeks of enzalutamide administration. Overall survival (OS) after enzalutamide among men with50% decline at 4 weeks was significantly better than that among men with a PSA decline50% (not reached vs. 34 months, p=0.008). OS after first-line abiraterone treatment for men with PSA decline50% and50% was not reached and 46 months, respectively (p=0.007). A PSA decline of50% at 4 weeks of enzalutamide administration was an independent predictor of longer OS.A PSA decline of50% at 4 weeks after the start of sequential enzalutamide treatment following abiraterone treatment predicted long-term survival in patients with mCRPC. Early PSA decline can identify patients who benefit from second-line enzalutamide after abiraterone treatment and can be useful as a decision-making tool regarding treatment.

BACKGROUND: Androgen receptor (AR) activation has been implicated in the pathogenesis of urothelial cancer. However, it remains controversial whether 5α-reductase inhibitors (5α-RIs), which are known for blocking the conversion of testosterone to the more potent androgen dihydrotestosterone and often prescribed for the treatment of, for instance, benign prostatic hyperplasia, contribute to preventing the development of bladder cancer. OBJECTIVE: To determine the role of 5α-RI therapy in urothelial tumorigenesis and tumor progression, using cell line models. METHODS: In a human non-neoplastic urothelial SVHUC subline stably expressing a full-length wild-type human AR (SVHUC-AR) with carcinogen/MCA challenge and human bladder cancer lines, we assessed the effects of three 5α-RIs, dutasteride (up to 100 nM), finasteride (up to 500 nM), and epristeride (up to 5μM), on neoplastic/malignant transformation and cell growth, respectively. RESULTS: In AR-positive bladder cancer UMUC3 and 5637-AR cells, an AR antagonist bicalutamide significantly inhibited their proliferation, whereas three 5α-RIs failed to do. Similarly, these 5α-RIs did not significantly inhibit the migration of bladder cancer cells induced by the treatment of testosterone which could be metabolized into dihydrotestosterone in culture medium. In MCA-SVHUC-AR cells, induction of their neoplastic transformation by testosterone, which was prevented by bicalutamide, was confirmed. However, no significant inhibitory effects of 5α-RIs on the neoplastic transformation of AR-positive urothelial cells treated with or without testosterone were observed. CONCLUSIONS: Using in vitro models for urothelial cancer, 5α-RI treatment even at supra-pharmacological doses was thus found to have no significant impact on the prevention of both tumorigenesis and tumor progression.

We found that FOXO1-shRNA sublines or FOXO1-positive cells co-treated with a FOXO1 inhibitor were significantly more resistant to cisplatin treatment at pharmacological concentrations, compared with respective control sublines or those with mock treatment. Western blot demonstrated considerable increases in the expression levels of a phosphorylated inactive form of FOXO1 (p-FOXO1) in cisplatin-resistant sublines established by long-term culture with low/increasing doses of cisplatin, compared with respective controls. Immunohistochemistry in surgical specimens from patients with muscle-invasive bladder cancer undergoing cisplatin-based neoadjuvant therapy further showed a strong trend to associate between p-FOXO1 positivity and unfavorable response to chemotherapy.

We examined the prognostic use of the 3-month prostate-specific antigen (PSA3m) level after androgen-deprivation therapy in patients with de novo metastatic hormone-sensitive prostate cancer (mHSPC).The present study included 145 patients with mHSPC who received primary androgen-deprivation therapy.The optimal cutoff PSA3m value for prediction of 5-year overall survival was 2.56 ng/ml (area under the receiver operating characteristics curve=0.67) using a time-dependent receiver operating characteristic (survival ROC) curve. In patients with CHAARTED low-volume and LATITUDE low-risk disease, the median overall survival was longer for patients with low PSA3m than that for those with high PSA3m. Multivariate analysis revealed PSA3m (hazard ratio=1.99; p=0.006) and age ≥80 years as independent risk factors for overall survival in patients with mHSPC.PSA3m can be a useful prognostic biomarker to avoid excessive upfront combination therapy, particularly in elderly patients with low-volume and low-risk mHSPC.

INTRODUCTION AND OBJECTIVE:We and others have indicated that androgen receptor (AR) signaling plays a critical role in urothelial cancer outgrowth. Meanwhile, our DNA microarray data suggest that l...

Background/Aim: To clarify the clinical significance of the temporary elevated C-reactive protein (CRP) levels followed by a decrease below baseline (CRP flare response) after administration of pembrolizumab to patients with advanced urothelial carcinoma (UC). Patients and Methods: We retrospectively reviewed 31 patients with advanced UC who received pembrolizumab. Patients were categorized into 3 groups (flare-responder, responder, non-responder) according to early CRP kinetics. Intergroup tumor response and survivals were compared. Results: Objective response rates of flare-responder, responder, and non-responder groups were 75%, 80%, and 26%, respectively. Median overall survival was not reached in flare-responder and responder groups, and was 10.2 months in the non-responder group (p=0.03). Furthermore, the flare-responder group did not reach median progression-free survival, and for the responder and non-responder groups it was 15.2 and 2.8 months, respectively (p=0.03). Conclusion: CRP flare response might be a promising biomarker in patients with advanced UC who received pembrolizumab.

Remarkable developments in the treatment of metastatic castration-resistant prostate cancer (mCRPC) have been achieved over the past decade. Although targeting the novel androgen receptor axis and using chemotherapeutic agents have improved survival, mCRPC is still a lethal disease. A better molecular characterization of cancer resulted in the determination of the important role of homologous recombination repair (HRR) genes in cancer development, and poly (ADP-ribose) polymerase (PARP) is one of the most attractive therapeutic targets. Recent clinical studies have demonstrated that PARP inhibitors significantly improve oncological outcomes in patients with mCRPC harboring BRCA mutations, and PARP inhibitors are becoming a standard of care for these patients. However, not only PARP inhibitors, but also chemotherapeutic agents such as platinum agents, taxanes, and radium-223 are active in HRR gene mutation carriers, and platinum sensitivity may predict the efficacy of PARP inhibitors for mCRPC. The combination of PARP inhibitors with other anti-cancer agents may overcome resistance mechanisms against PARP inhibitors and lead to survival benefits. Appropriate treatment sequences and combinations may change the therapeutic landscape of DNA repair deficient mCRPC.

Simple Summary It remains unclear why chemotherapy is often ineffective in patients with bladder cancer. Meanwhile, we previously reported that male sex hormones (i.e., androgens) could considerably reduce the efficacy of cisplatin, an anti-cancer drug used as the first-line treatment against advanced bladder cancer. The present study aimed to investigate how androgen receptor signaling, which is activated by binding of androgenic hormones, modulates sensitivity to cisplatin treatment in bladder cancer, using cell line models and surgical specimens. We found that the expression levels of the androgen receptor and a molecule (BXDC2) were inversely correlated and that loss of BXDC2 was associated with cisplatin resistance. We thus provide evidence to suggest an underlying molecular mechanism responsible for androgen receptor-induced chemoresistance in bladder cancer. Abstract Underlying mechanisms for resistance to cisplatin-based chemotherapy in bladder cancer patients are largely unknown, although androgen receptor (AR) activity, as well as extracellular signal-regulated kinase (ERK) signaling, has been indicated to correlate with chemosensitivity. We also previously showed ERK activation by androgen treatment in AR-positive bladder cancer cells. Because our DNA microarray analysis in control vs. AR-knockdown bladder cancer lines identified BXDC2 as a potential downstream target of AR, we herein assessed its functional role in cisplatin sensitivity, using bladder cancer lines and surgical specimens. BXDC2 protein expression was considerably downregulated in AR-positive or cisplatin-resistant cells. BXDC2-knockdown sublines were significantly more resistant to cisplatin, compared with respective controls. Without cisplatin treatment, BXDC2-knockdown resulted in significant increases/decreases in cell proliferation/apoptosis, respectively. An ERK activator was also found to reduce BXDC2 expression. Immunohistochemistry showed downregulation of BXDC2 expression in tumor (vs. non-neoplastic urothelium), higher grade/stage tumor (vs. lower grade/stage), and AR-positive tumor (vs. AR-negative). Patients with BXDC2-positive/AR-negative muscle-invasive bladder cancer had a significantly lower risk of disease-specific mortality, compared to those with a BXDC2-negative/AR-positive tumor. Additionally, in those undergoing cisplatin-based chemotherapy, BXDC2 positivity alone (p = 0.083) or together with AR negativity (p = 0.047) was associated with favorable response. We identified BXDC2 as a key molecule in enhancing cisplatin sensitivity. AR-ERK activation may thus be associated with chemoresistance via downregulating BXDC2 expression in bladder cancer.

We recently demonstrated that silodosin, a selective α(1)-blocker often prescribed for the symptomatic treatment of benign prostatic hyperplasia (BPH), could inactivate a c-fos proto-oncogene regulator ELK1 in bladder cancer cells possessing a functional androgen receptor (AR). However, the clinical impact of α(1)-blockers on the development and progression of bladder cancer remained poorly understood. In the present study, we investigated if α(1)-blockers clinically used, including silodosin, tamsulosin, and naftopidil, could prevent the neoplastic/malignant transformation and cell growth, using non-neoplastic urothelial SVHUC sublines with carcinogen/MCA challenge and bladder cancer lines, respectively. Bladder cancers in men treated with silodosin, tamsulosin, or naftopidil for their BPH were then compared. Silodosin at 1-10 µM significantly inhibited the neoplastic transformation of MCA-SVHUC-AR cells, but not that of AR-negative MCA-SVHUC-control cells. In MCA-SVHUC-AR, silodosin significantly reduced the expression levels of oncogenes (c-fos/NF-κB1) and induced those of tumor suppressors (p27/PTEN). However, tamsulosin (up to 1 µM) or naftopidil (up to 10 µM) failed to significantly inhibit the neoplastic transformation of AR-positive or AR-negative urothelial cells. Similarly, cell proliferation/migration of AR-positive bladder cancer lines was considerably inhibited only by silodosin. Meanwhile, the incidence of bladder cancer in patients with silodosin [49/540 (9.1%)] was marginally lower, compared to those with tamsulosin [64/523 (12.2%); P=0.094] or tamsulosin or naftopidil [64+28/523+236 (12.1%); P=0.082]. There were no significant differences in tumor grade/stage among the 3 cohorts. Outcome analysis revealed lower risks for disease progression of non-muscle-invasive bladder tumors in the silodosin group than in the naftopidil group (P=0.011) or tamsulosin+naftopidil groups (P=0.035). Similarly, silodosin patients with muscle-invasive tumor had lower risks for disease progression, compared with tamsulosin (P=0.006) or tamsulosin+naftopidil (P=0.028) patients. Multivariate analysis further showed that silodosin treatment in those with non-muscle-invasive tumor was associated with improved progression-free survival, compared with naftopidil (hazard ratio=0.086; 95% confidence interval=0.008-0.905; P=0.041) or tamsulosin/naftopidil (hazard ratio=0.128; 95% confidence interval=0.016-1.036; P=0.054) treatment. Our in vitro studies thus indicate that both urothelial tumorigenesis and tumor growth are inhibited by silodosin, but not by tamsulosin or naftopidil. Clinical data further suggest that even pharmacological doses (e.g. 0.1 µM) of silodosin contribute to preventing bladder cancer progression.

The efficacy of cisplatin-based chemotherapy in patients with bladder cancer is often limited due to the development of therapeutic resistance. Our recent findings in bladder cancer suggested that activation of prostaglandin receptors (

A steroid hormone receptor, mineralocorticoid receptor (MR), is well known to play a critical role in maintaining normal homeostasis in the body primarily via regulating ionic and water transports. Indeed, MR antagonists have been prescribed to the patients as diuretic drugs. Meanwhile, emerging evidence has indicated that MR signaling, with or without functional interplay with glucocorticoid receptor or androgen receptor, contributes to modulating the development and progression of several types of neoplasms including genitourinary malignancies. This review summarizes the available data suggesting the involvement of MR signaling in renal cell carcinoma, prostatic adenocarcinoma, urothelial carcinoma, and other malignancies, and highlights potential underlying molecular mechanisms.

The results of ab−initio electronic structure calculations, X-ray diffraction, magnetic, and 151Eu Mossbauer spectroscopy investigations of the EuRhO3 orthorhodite are presented. The orthorhodite is shown to crystallize in the orthorhombic space group Pnma and its lattice constants are a = 5.7499(1) A, b = 7.6863(1) A, and c = 5.3095(1) A. The electron charge density distributions point toward the presence of a mixture of ionic and directional covalent bonding. A detailed analysis of the density of states and the energy band structure reveals half-metallic/half-insulator characteristics of EuRhO3. The Eu atoms in EuRhO3 are shown to be in the trivalent oxidation state. It is demonstrated that EuRhO3 is a paramagnet down to 2.3 K. The Debye temperature of EuRhO3 is found to be 254(3) K.

The results of X-ray diffraction, magnetic, and 155 Gd Mossbauer spectroscopy study, complemented by the a b - i n i t i o electronic structure and the hyperfine-interaction parameters calculations, of the GdRhO 3 orthorhodite are reported. GdRhO 3 crystallizes in the orthorhombic space group P n m a with the lattice parameters a = 5.7450 ( 1 ) A, b = 7.6647 ( 1 ) A, and c = 5.2905 ( 1 ) A. The evidence is provided for the presence of directional covalent bonding between the Rh and O atoms and of ionic bonding between the Gd and Rh/O atoms. GdRhO 3 orders antiferromagnetically with the Neel temperature T N = 2.13 ( 5 ) K. The magnetic susceptibility above T N follows the modified Curie-Weiss law with the paramagnetic Curie temperature of − 3.37 ( 1 ) K and the effective magnetic moment of 7.99(1) μ B per Gd atom. The Debye temperature of GdRhO 3 determined from the Mossbauer data is found to be 256(1) K. The calculated Gd magnetic moment and hyperfine-interaction parameters are in good agreement with the experimental values.

Androgen receptor (AR) and estrogen receptor-β (ERβ) have been implicated in urothelial tumor outgrowth as promoters, while underlying mechanisms remain poorly understood. Our transcription factor profiling previously performed identified FOXO1 as a potential downstream target of AR in bladder cancer cells. We here investigated the functional role of FOXO1 in the development and progression of urothelial cancer in relation to AR and ERβ signals. In non-neoplastic urothelial SVHUC cells or bladder cancer lines, AR/ERβ expression or dihydrotestosterone/estradiol treatment reduced the expression levels of FOXO1 gene and induced those of a phosphorylated inactive form of FOXO1 (p-FOXO1). In chemical carcinogen-induced models, FOXO1 knockdown via shRNA or inhibitor treatment resulted in considerable induction of the neoplastic transformation of urothelial cells or bladder cancer development in mice. Similarly, FOXO1 inhibition considerably induced the viability, migration, and invasion of bladder cancer cells. Importantly, in FOXO1 knockdown sublines, an anti-androgen hydroxyflutamide or an anti-estrogen tamoxifen did not significantly inhibit the neoplastic transformation of urothelial cells, while dihydrotestosterone or estradiol did not significantly promote the proliferation or migration of urothelial cancer cells. In addition, immunohistochemistry in surgical specimens showed that FOXO1 and p-FOXO1 expression was down-regulated and up-regulated, respectively, in bladder tumor tissues, which was further associated with worse patient outcomes. AR or ERβ activation is thus found to correlate with inactivation of FOXO1 which appears to be their key downstream effector. Moreover, FOXO1, as a tumor suppressor, is likely inactivated in bladder cancer, which contributes in turn to inducing urothelial carcinogenesis and cancer growth.

The utility of frozen section analysis (FSA) during partial cystectomy has not been established. We assessed the impact of intraoperative FSA in partial cystectomy cases on surgical margin (SM) status and patient outcome.A retrospective review identified 76 consecutive patients who underwent partial cystectomy for bladder carcinoma with (n = 66; 87%) or without (n = 10; 13%) FSA for SMs at our institution from 2004 to 2018. FSA was correlated with the diagnosis of the frozen section control, the status of final SM, and the prognosis.Final SM was positive in 9 (12%) cystectomies, including 6 (9%) FSA vs. 3 (30%) non-FSA cases (P = 0.091). There were no significant differences in tumor size, histology, or tumor grade/stage between the 2 cohorts. FSAs were reported as positive (n = 7; 11%), atypical (n = 10; 15%), and negative (n = 49; 74%). All of the positive and negative FSA diagnoses were confirmed accurate on the frozen section controls, whereas atypical diagnoses were revised to benign (n = 4), atypical (n = 4), and carcinoma (n = 2) on the controls. Ten (77%) of 13 initial FSA-positive (6 of 7)/atypical (4 of 6; excluding benign diagnoses on the controls) cases achieved negative conversion by excision of additional tissue. Thus, final SM was positive in 1 (14%) FSA-positive case, 3 (30%) FSA-atypical cases (including one at the SM where FSA was not sampled), and 2 (4%) FSA-negative cases (at the SM where FSA was not sampled). Kaplan-Meier analysis and log-rank test revealed an association of performing FSA with the risk of disease progression (P = 0.021), but not intravesical recurrence (P = 0.434) or cancer-specific mortality (P = 0.560). Initial positive/atypical FSA, as an independent prognosticator, was associated with reduced progression-free (P = 0.002) and cancer-specific (P = 0.004) survival rates, compared with initial negative FSA. Positive SM was also associated with a larger tumor size (P0.05) and a higher risk of intravesical recurrence (P = 0.070) or disease progression (P = 0.096).Performing FSA during partial cystectomy may contribute to preventing positive SM and disease progression. Additionally, as seen in most of initial FSA-positive/atypical cases that achieved negative conversion, select patients may benefit from the routine FSA. Meanwhile, positive or atypical FSA was associated with significantly poorer prognosis.

A new method for the crystal growth of alkaline-earth palladate CaPd3O4 was developed. The crystals were synthesized on a voltage-applied electrode in a molten chloride solvent. The maximum length of the crystal was about 1.5 mm. The X-ray diffraction data were refined well by assuming a cubic structure of the space group Pm n, and the lattice constant a was 5.7471 (10) ?. The temperature dependence of the resistivity showed semiconductor-like characteristics with a very small activation energy Ea of 0.45 meV at low temperatures, and the resistivity at 300 K was 0.1 cm. The temperature dependence of the molar magnetic susceptibility showed the Curie-Weiss paramagnetic behavior with a small molar Curie constant Cmol of 5.0(1) × 10-3 emu K/(mol Oe), indicating the existence of localized spin moments.

Crystals of ternary LnRu2P2 (Ln = Pr, Nd, Sm, Tb, Dy, Er) systems were synthesized, and their crystallographic, magnetic, and electric properties were investigated. All the crystals have a tetragonal ThCr2Si2-type structure of space group I4/mmm. The lattice constants decrease as the number of 4f electrons increases, reflecting the lanthanide contraction. An antiferromagnetic transition was observed for LnRu2P2 (Ln = Pr, Nd, Sm, Tb, Dy) at 25 K (Pr), 19 K (Nd), 15 K (Sm), 22.5 K (Tb), and 13 K (Dy). However, no transition was observed for ErRu2P2 down to 5 K. The Peff agrees well with the theoretical moment g J ( J + 1 ) of lanthanides, suggesting that lanthanides make a major contribution to the magnetic moment of LnRu2P2. A spin-flop-like transition was observed in the M(H) curves of PrRu2P2 and TbRu2P2 at 4 and 8 kOe, respectively; however, no saturation was observed up to 55 kOe.

Synthesis and characterization of Sr1−xAxPd3O4 (A = Na, Bi) are reported. All the doped phases crystallize in the cubic symmetry with the space group Pm3m. Both Hall and thermopower measurement results indicate that substitutions of Na+ and Bi3+ into the Sr2+ site introduce hole and electron carriers, respectively. As the dopant concentration increases, effective magnetic moment, electrical conductivity and carrier concentration of these phases increase and thermopower decreases. The highest power factor obtained among these doped samples is 0.5 μW/K2 cm at room temperature for Sr0.8Na0.2Pd3O4.

A series of orthorhombic NaLnTiO 4 (Ln = lanthanides) has been synthesized and characterized. These compounds all crystallize in A-site ordered n = 1 Ruddlesden–Popper phase (A n +1 B n O 3 n +1 ) structure. The weak ferromagnetism with large magnetization has been observed for Ln = Tb and Dy, and non-linear field dependence of magnetization without hysteresis has been observed for Ln = Er and Ho. By performing the symmetry operations, two possible canted spin arrangements have been proposed.

Ln 2 BaPdO 5 (Ln = La, Pr, Nd, Sm, Eu, Gd, Dy, Ho) all crystallizes in Nd 2 BaZnO 5 structure which is proposed to have a Shastry–Sutherland (S–S) lattice of Ln 3+ ions. Ln 2 BaPdO 5 (Ln = Nd, Sm, Gd, Dy, Ho) exhibits antiferromagnetic transitions at temperatures between 2 and 5 K. In addition, metamagnetic transitions have been observed for Ln 2 BaPdO 5 (Ln = Nd, Dy, Ho) below 2 K. Specific heat of Ln 2 BaPdO 5 (Ln = Ho, Dy) exhibits symmetric peaks at T N , and residual entropy below T N is negligibly small. On the contrary, specific heat of Ln 2 BaPdO 5 (Ln = Nd, Sm, Gd) exhibits Schottky type anomalies followed by sharp peaks at T N , and residual entropy below T N is large. From these results, the applicability of the S–S model to Ln 2 BaPdO 5 with various Ln 3+ ions is proposed.

Single-phase polycrystalline samples of PbPdO 2 have been synthesized via solid-state reaction, and their electrical, magnetic and thermoelectric properties have been characterized. The temperature-dependent dc electrical resistivity exhibits metal–insulator transition around 90 K. Thermoelectric power and Hall effect measurement results indicate that the majority of carriers in PbPdO 2 are holes. The thermoelectric power is 95 μV/K at 290 K and large for metallic materials. Based on the temperature proportionality of thermoelectric power, PbPdO 2 is essentially a metal. The insulating behavior at low temperatures is driven by localization of charge carriers manifested by Curie paramagnetism.

We made study of the comparative characteristic of transparent organic light emitting diodes by using three kinds of typical transparent conducting oxide ( ITO (In2O3-SnO2), IZO (In2O3-ZnO), AZO (ZnO-Al2O3) ). The cathode used for transparent conducting oxide were prepared by rf magnetron sputtering at room temperature. Each transparent conduction film was amorphous. We also study the effects of using alkali metal (Cs) dope layer. An electronic injection improved by doping Cs, and the decrease in driving voltage of TOLED and the improvement of luminance were observed.