Microscopic annealing process and its impact on superconductivity in T'-structure electron-doped copper oxides

High-transition-temperature superconductivity arises in copper oxides when holes or electrons are doped into the CuO2 planes of their insulating parent compounds. While hole-doping quickly induces metallic behavior and superconductivity in many cuprates, electron-doping alone is insufficient in materials such as R2CuO4 (R is Nd, Pr, La, Ce, etc.), where it is necessary to anneal an as-grown sample in a low-oxygen environment to remove a tiny amount of oxygen in order to induce superconductivity. Here we show that the microscopic process of oxygen reduction repairs Cu deficiencies in the as-grown materials and creates oxygen vacancies in the stoichiometric CuO2 planes, effectively reducing disorder and providing itinerant carriers for superconductivity. The resolution of this long-standing materials issue suggests that the fundamental mechanism for superconductivity is the same for electron- and hole-doped copper oxides.Comment: 23 pages, 3 figures, accepted for publication in Nature Material

Breast Cancer in Hong Kong, Southern China: The First Population-Based Analysis of Epidemiological Characteristics, Stage-Specific, Cancer-Specific, and Disease-Free Survival in Breast Cancer Patients: 1997–2001

Background: Cancer registries have been set up worldwide to provide information for cancer health planning. There are known variations in breast cancer incidence and mortality worldwide. However, breast cancer incidence, pathological characteristics, and survival data is still underreported in Asian countries. This is the first comprehensive population-based breast cancer study performed using population database of the Hong Kong Cancer Registry. Methods: A retrospective review of medical records of 8,961 subjects who were diagnosed with breast cancer between January 1, 1997 to December 31, 2001 and followed up to December 31, 2007. Descriptive statistics were employed to analyze the epidemiological and clinical data. Estimates of overall, disease-free, and cancer-specific survival at 5 years were estimated by the Kaplan-Meier method and stage-specific relative survival rates were calculated. Results: A total of 7,630 breast cancer patients' medical records and dataset were available during this period, and 7,449 subjects were eligible for the final analysis. Median follow-up was 84 months. A total of 47.4% were diagnosed with breast cancer at age 49 years and younger;22.2%, 46.9%, 10.8%, and 4.1% presented at stages I, II, III, and IV, respectively. A total of 53.5% had ER-positive cancer, and 20.3% had HER2-positive cancers;13.4% had triplenegative cancers. The relative, cancer-specific, and diseasefree survival rates at 5 years were 84%, 85.2%, and 81.2%, respectively. Discussion. We performed the first comprehensive population-based breast cancer epidemiology study in Southern China using the Hong Kong Cancer Registry database. This provides a baseline study cohort for comparative studies with other Asian countries and Chinese who have migrated to the West. © The Author(s) 2011. This article is published with open access at Springerlink.com.published_or_final_versionSpringer Open Choice, 21 Feb 201

Prostate Cancer Induced by Loss of Apc Is Restrained by TGFβ Signaling

Recent work with mouse models of prostate cancer (CaP) has shown that inactivation of TGFβ signaling in prostate epithelium can cooperate with deletion of the Pten tumor suppressor to drive locally aggressive cancer and metastatic disease. Here, we show that inactivating the TGFβ pathway by deleting the gene encoding the TGFβ type II receptor (Tgfbr2) in combination with a deletion of the Apc tumor suppressor gene specifically in mouse prostate epithelium, results in the rapid onset of invasive CaP. Micro-metastases were observed in the lymph nodes and lungs of a proportion of the double mutant mice, whereas no metastases were observed in Apc single mutant mice. Prostate-specific Apc;Tgfbr2 mutants had a lower frequency of metastasis and survived significantly longer than Pten;Tgfbr2 double mutants. However, all Apc;Tgfbr2 mutants developed invasive cancer by 30 weeks of age, whereas invasive cancer was rarely observed in Apc single mutant animals, even by one year of age. Further comparison of the Pten and Apc models of CaP revealed additional differences, including adenosquamous carcinoma in the Apc;Tgfbr2 mutants that was not seen in the Pten model, and a lack of robust induction of the TGFβ pathway in Apc null prostate. In addition to causing high-grade prostate intra-epithelial neoplasia (HGPIN), deletion of either Pten or Apc induced senescence in affected prostate ducts, and this restraint was overcome by loss of Tgfbr2. In summary, this work demonstrates that TGFβ signaling restrains the progression of CaP induced by different tumor suppressor mutations, suggesting that TGFβ signaling exerts a general tumor suppressive effect in prostate.This work was supported by a Program Project Grant from the National Cancer Institute (2P01CA104106 to B. Paschal and D. Wotton), and by a pilot grant from the UVA Cancer Center (funded from the CCSG P30 CA44579, the James and Rebecca CraigFoundation, and UVA Women's Oncology fund) to D. Wotton. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Sharon Birdsall for technical assistance, Anindya Dutta and Dan Gioeli for helpful discussions, and Chun-Song Yang for advice and reagent