Improving the Safety and Effectiveness of Contraception in China: a Case-Study in Promotion and Improvement of Family Planning
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Anordrin Eliminates Tamoxifen Side Effects Without Changing Its
www.nature.com/scientificreports OPEN Anordrin Eliminates Tamoxifen Side Effects without Changing Its Antitumor Activity Received: 26 August 2016 Wenwen Gu1,*, Wenping Xu2,*, Xiaoxi Sun3, Bubing Zeng2, Shuangjie Wang1, Nian Dong4, Accepted: 31 January 2017 Xu Zhang1, Chengshui Chen4, Long Yang5, Guowu Chen3, Aijie Xin3, Zhong Ni6, Jian Wang1 & Published: 07 March 2017 Jun Yang1 Tamoxifen is administered for estrogen receptor positive (ER+) breast cancers, but it can induce uterine endometrial cancer and non-alcoholic fatty liver disease (NAFLD). Importantly, ten years of tamoxifen treatment has greater protective effect against ER+ breast cancer than five years of such treatment. Tamoxifen was also approved by the FDA as a chemopreventive agent for those deemed at high risk for the development of breast cancer. The side effects are of substantial concern because of these extended methods of tamoxifen administration. In this study, we found that anordrin, marketed as an antifertility medicine in China, inhibited tamoxifen-induced endometrial epithelial cell mitosis and NAFLD in mouse uterus and liver as an anti-estrogenic and estrogenic agent, respectively. Additionally, compared with tamoxifen, anordiol, the active metabolite of anordrin, weakly bound to the ligand binding domain of ER-α. Anordrin did not regulate the classic estrogen nuclear pathway; thus, it did not affect the anti- tumor activity of tamoxifen in nude mice. Taken together, these data suggested that anordrin could eliminate the side effects of tamoxifen without affecting its anti-tumor activity. Tamoxifen was the first FDA-approved drug for breast cancer patients with positively expressed estrogen recep- tors (ER)1. However, tamoxifen also induces side effects, such as uterine endometrial cancer and non-alcoholic fatty liver disease (NAFLD). -
Threat to the PHLS
Br Med J (Clin Res Ed): first published as 10.1136/bmj.290.6468.579 on 23 February 1985. Downloaded from LONDON, SATURDAY 23 FEBRUARY 1985 MEDICAL JOURNAL Threat to the PHLS In its drive for economy the government has included among Furthermore, the creation of the Communicable Disease its targets the Public Health Laboratory Service of England Surveillance Centre by the PHLS on behalfofthe DHSS and and Wales. The proposal under consideration is the transfer the Welsh Office has required additional epidemiological of some (or possibly all) the Service's 52 regional and area resources for the national surveillance and control of laboratories to the control of health authorities. The argu- communicable disease, functions previously performed by ment seems to be that in the existing joint PHLS-hospital the departments. The laboratory reporting system has been laboratories most of the specimens examined are for the expanded with contributions from hospital laboratories, diagnosis of infection in individual patients, so that it would individual consultants, and the Royal College of General be logical to transfer these laboratories to the control of the Practitioners helping to provide a fuller epidemiological National Health Service. picture. Many more field investigations of outbreaks have The joint PHLS-hospital laboratories became the pattern been undertaken, as publications in the BMJ have shown. in the 1960s by agreement between the PHLS and the The result has been an unfortunate decline in the multicentre Department ofHealth and Social Security. The reasons were studies and epidemiological research for which the PHLS partly economic but mainly because joint laboratories alone structure is particularly suited. -
Reproductive Health Guideline Appendix 3 – Search Strategies
SUPPLEMENTARY APPENDIX 3: Search Strategies 2020 American College of Rheumatology Guideline for the Management of Reproductive Health in Rheumatic and Musculoskeletal Diseases All searches initially run on 11/8/2017 and updated on 5/8/2018. Searches run from database inception to 5/8/2018. PUBMED Syntax Guide for PubMed [MeSH] = Medical Subject Heading [Text Word] = Includes all words and numbers in the title, abstract, other abstract, MeSH terms, MeSH Subheadings, Publication Types, Substance Names, Personal Name as Subject, Corporate Author, Secondary Source, Comment/Correction Notes, and Other Terms - typically non-MeSH subject terms (keywords)…assigned by an organization other than NLM [MeSH subheading] = a Medical Subject [Title/Abstract] = Includes words in the title Heading subheading, e.g. -
Effect of A-Nor Steroids and Oestradiol on Progesterone Production By
Effect of A-nor steroids and oestradiol on progesterone production by human luteal cells Wang Han-zheng, Lu Shu-hua, Shen Wei-xiong, Sun Zhi-da, Zhou Wei, Wu Yu-fen and Zhou Mei-rong Shanghai Institute of Planned Parenthood Research, *Shanghai Lu-wan District Maternity and Child Health Hospital and fRen-jin Hospital, Shanghai No. 2 Medical University, Shanghai, China Summary. Cell suspensions were prepared from human corpora lutea obtained during the mid-luteal phase. Progesterone production was assessed after short-term incubation of luteal cell suspensions. Luteal cells were very sensitive to hCG, the concentration required for 50% maximum response being 0\m=.\01i.u./ml, and the response was 5 times higher than the basal production. Oestradiol (1\p=n-\100\g=m\m)induced a significant dose-related decrease in both basal and hCG-stimulated progesterone production. The A-nor steroidal compounds anordrin and AF-45 reduced hCG-stimulated progesterone production only at the high concen- tration of 100 \g=m\m.The ED50 values were approximately 3 \g=m\m,75 \g=m\mand 100 \g=m\mfor oestradiol, AF-45 and anordrin respectively. Anordrin showed no significant effects on basal progesterone production. In addition, oestradiol markedly inhibited the activity of 3\g=b\-hydroxysteroiddehydrogenase in luteal cells, expressed by the conversion of pregnenolone to progesterone, but the inhibitory effects of anordrin and AF-45 were negligible or relatively low. The effects of anordrin and AF-45 were different from those of oestradiol on pro- gesterone production by human luteal cells in vitro, indicating that neither substance is likely to be a useful luteolytic agent in women. -
Induction of Apoptosis of Human Leukemia Cells by α
Chinese Journal of Cancer Research 9(1):1-5,199Z Basic Investigations INDUCTION OF APOPTOSIS OF HUMAN LEUKEMIA CELLS BY ¢x-ANORDRIN Lou Liguang ~J~-~f- Xu Bin ~j:~ Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 200031 The apoptosis-inducing effect of c¢-anordrin (ANO) human promyelocytic leukemia HL-60 cells. 3 was investigated in this study. ANO 10-50 ttM inhibited However, the mechanism of its antitumor activity was the growth of both human leukemia HL-60 and I(,562 still unclear. In this work, we further investigated the cells by 19-52%. Electron microscopy showed that tumor-inhibitory effect of ANO to explore the possible ANO-treated cells exhibited the drastic changes including mechanisms of its action. cell shrinkage, chromatin condensation, nuclear frag- mentation, typical of apoptosis. Gel electrophoresis of DNA extracted from both HI~60 and K562 cells treated MATERIALS AND METHODS with ANO revealed characteristic "ladder" pattern. ANO 50 IxM for 48 h caused approximately 50=70% Drug apoptosis. Cycloheximide (CHX) and actinomycin D (Act D) did not prevent ANO-induced apoptosis in K562 ANO was produced by Shanghai No. 19 cells, however, apoptosis of HL-60 cells in the presence of Pharmaceutical Factory and purified in our institute. 4 ANO was partially blocked by these two agents. Its stock solution was made in ethanol at the Moreover, it was found that tamoxifen synergically concentration of 50 mM. The final concentration of potentiated and estradiol partially antagonized ANO- ethanol was less than 0.1% which had no significant induced apoptosis in HL-60 cells. -
WO 2015/169173 Al 12 November 2015 (12.11.2015) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2015/169173 Al 12 November 2015 (12.11.2015) P O P C T (51) International Patent Classification: (74) Agent: CHINA SINDA INTELLECTUAL PROPERTY A61K 31/56 (2006.01) A61P 3/04 (2006.01) LTD.; B l 1th Floor, Focus Place, 19 Financial Street, A61P 35/00 (2006.01) A61P 3/06 (2006.01) Xicheng District, Beijing 100033 (CN). A61P 15/12 (2006.01) A61P 19/10 (2006.01) (81) Designated States (unless otherwise indicated, for every A61P 1/16 (2006.01) kind of national protection available): AE, AG, AL, AM, (21) International Application Number: AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, PCT/CN20 15/077942 BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 30 April 2015 (30.04.2015) KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, (25) Filing Language: English MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, (26) Publication Language: English SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, (30) Priority Data: TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. 2014 10192569.2 8 May 2014 (08.05.2014) CN (84) Designated States (unless otherwise indicated, for every (71) Applicants: SHANGHAI INSTITUTE OF PLANNED kind of regional protection available): ARIPO (BW, GH, PARENTHOOD RESEARCH [CN/CN]; 2140 Xietu GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, Road, Building#2, Room 502, Xuhui District, Shanghai TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, 200032 (CN). -