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β-Catenin Mutations and Protein Accumulation in All Hepatoblastomas Examined from B6C3F1 Mice Treated with Anthraquinone or Oxazepam
Colleen H. Anna, Robert C. Sills, Julie F. Foley, Patricia S. Stockton, Thai-Vu Ton and Theodora R. Devereux
Colleen H. Anna
Laboratories of Molecular Carcinogenesis [C. H. A., T. R. D.] and Experimental Pathology [R. C. S., J. F. F., P. S. S., T-V. T.], National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709
Robert C. Sills
Julie F. Foley
Patricia S. Stockton
Thai-Vu Ton
Theodora R. Devereux
DOI: Published June 2000
The molecular pathogenesis of hepatoblastomas in the B6C3F1 mouse is unclear but may involve alterations in the β-catenin/Wnt signaling pathway as was recently described for chemically induced hepatocellular neoplasms and human liver cancers. The objective of this study was to characterize the mutation frequency and spectrum of β-catenin mutations and the intracellular localization of β-catenin protein accumulation in chemically induced hepatoblastomas. In this study, β-catenin mutations were identified in all 19 anthraquinone-induced hepatoblastomas and all 8 oxazepam-induced hepatoblastomas examined. Although several hepatoblastomas had multiple deletion and/or point mutations, the pattern of mutations in the hepatoblastomas did not differ from that identified in hepatocellular neoplasms. In a majority of the hepatoblastomas (six of seven) examined by immunohistochemical methods, both nuclear and cytoplasmic localization of β-catenin protein were detected, whereas in hepatocellular adenomas, carcinomas, and normal liver only membrane staining was observed. Our data suggest that β-catenin mutations and the subsequent translocation of β-catenin protein from the cell membrane to the cytoplasm and nucleus may be critical steps in providing hepatocellular proliferative lesions with the growth advantage to progress to hepatoblastomas.
An increased incidence of highly malignant hepatoblastomas has been observed in mice following treatment with certain chemicals in National Toxicology Program carcinogenesis studies (1 , 2) , whereas these tumors are rare in untreated mice. It has been hypothesized that these tumors arise from or are a rare variant of hepatocellular carcinomas (2) . Diwan et al. (3) found that hepatoblastomas in mice developed after exposure to promoters such as phenobarbital in initiation-promotion protocols. Few studies of molecular analyses on chemically induced hepatoblastomas have been reported, although H-ras activation and p53 mutation have not been found (4 , 5) .
Hepatoblastomas are the most frequent malignant liver tumor found in young children (6) . There is also an increased incidence of these tumors in patients with APC 2 who carry a germline mutation in the APC gene, and recently it was discovered that there is a high frequency of β-catenin mutations and β-catenin protein accumulation in sporadic hepatoblastomas (7) .
β-catenin is a central and critical molecule in the Wnt signaling pathway. The APC gene product and the glycogen serine-threonine kinase-3β together target β-catenin for degradation and modulate its expression (8 , 9) . In some cancers, including colon and hepatocellular tumors, mutations in either APC or β-catenin lead to β-catenin protein accumulation and up-regulation of Wnt signaling, resulting ultimately in cell proliferation and inhibition of apoptosis (10) . During this process, cytoplasmic β-catenin may form a complex with Tcf transcription factors, enter the nucleus, and target genes such as c-MYC for transcription (9, 10, 11) .
β-catenin mutations have been identified at high frequency in human hepatocellular carcinomas (12) and in hepatocellular adenomas and carcinomas of mice exposed to certain chemicals (13 , 14) . In this study, we examined hepatoblastomas, which developed in mice treated with anthraquinone or oxazepam for 2 yr, for mutations in β-catenin. Anthraquinone is used in the manufacture of dyes and pigment and in the pulp and paper industry, and oxazepam is a commonly prescribed tranquilizer. We were particularly interested in whether the β-catenin mutation frequency or spectrum was chemical specific and whether the mutations in hepatoblastomas differed from those of hepatocellular adenomas or carcinomas. Therefore, we also assessed the mutation frequency and profile in hepatocellular neoplasms from B6C3F1 mice treated with anthraquinone. Laser capture microdissection was used to collect cells from some of the smaller hepatoblastomas to avoid contamination with surrounding normal tissue or adjacent hepatocellular tumors. In addition, we compared the protein expression and intracellular localization of β-catenin protein in hepatoblastomas and hepatocellular neoplasms.
Tumor Samples and DNA Isolation.
Oxazepam treatment, liver tumor collection, tumor incidence data of B6C3F1 mice, and H-ras oncogene mutation analysis for the studies have been reported previously (4) . The incidence of hepatoblastomas in male mice was 0%, 4%, 40%, and 24% at 0 ppm, 125 ppm, 2500 ppm, and 5000 ppm oxazepam, respectively; and for female mice, 0%, 2%, 16%, and 14%, respectively. For collection of liver tumors from the anthraquinone study B6C3F1 mice were fed diets containing 0, 833, 2500, or 7500 ppm anthraquinone for 105 weeks. The incidence of hepatoblastomas in male mice was 2%, 10%, 22%, and 43% at 0, 833, 2500, and 7500 ppm anthraquinone, respectively; and for female mice, only 2% at the 7500 ppm dose. A subset of the hepatocellular neoplasms and a small number of hepatoblastomas with surrounding tissue were frozen in liquid N2 and stored at −70°C. The remainder of the liver tissues was preserved in 10% neutral buffered formalin, trimmed, and embedded in paraffin. Sections 5–6 μm were used for staining with H&E. Normal liver, hepatoblastomas, and surrounding hepatocellular neoplasms (adenomas and carcinomas) were either hand-microdissected or laser capture microdissected (4 of 19 of the anthraquinone-induced hepatoblastomas) from 2–5 serial 10-μm paraffin sections for mutation analysis. A PixCell-I (30-μm spot size and about 500 hits/sample) LCM System (Arcturus Engineering Inc., Mountain View, CA) was used for the laser capture microdissection, as described previously (15 , 16) . Microdissected samples were digested overnight in 500 μl of digestion buffer [50 mm Tris (pH 8.5), 0.5% Tween 20, 1 mm EDTA, and 0.5 mg/ml proteinase K] at 55°C. DNA was obtained by boiling the digested samples for 5 min. In addition, most of the mutation analysis on the hepatocellular neoplasms was performed with DNA isolated from frozen tumor tissue, as described previously (4 , 16) .
β-Catenin Mutation Screening and Identification.
SSCP analysis was carried out on PCR products of exon 2 (corresponds to exon 3 in human) of the mouse β-catenin gene (12) , which contains the glycogen serine-threonine kinase-3β targeted phosphorylation sites within residues 33–45. The sequences of the intronic PCR primers flanking the borders of exon 2 were: BCAT-1F, 5′-TACAGGTAGCATTTTCAGTTCAC-3′; and BCAT-2R, 5′-TAGCTTCCAAACACAAATGC-3 (12) . Inner primers were BCAT-7F, 5′-TAACATACTCTGTTTTTACAGCTG-3′, and BCAT-8R, 5′-ACATCTTCTTCCTCAGGGTTG-3′. For DNA from frozen samples primers 1F × 2R were used for amplification. For DNA from fixed sections nested PCR was used with primers 1F × 2R for the outer reactions and both 1F × 8R and 7F × 8R for the inner reactions. [33P]-dATP was incorporated into the inner PCR reactions for SSCP analysis, and two gel conditions were used to detect mutations: 6% acrylamide gels with 10% glycerol were electrophoresed at 40 W for 6 h at 5°C, and 0.5× mutation detection enhancement (AT Biochem, Malvern, PA) gels were electrophoresed at 3 W for 17 h at room temperature. DNA from normal liver and no-DNA controls were included with all amplification experiments to confirm no cross-contamination of PCR products.
Point mutations and some small deletions were identified by reamplifying samples with altered bands on SSCP gels. Other deletions were identified by excision and boiling of the altered band, followed by a fresh amplification. The amplified bands were gel purified on Qiagen columns (Qiagen, Valencia, CA) before sequencing with a[ 33P]-Thermo-Sequenase kit (Amersham, Cleveland, OH) The amplification primers also served as sequencing primers. Mutation identification was confirmed with at least two amplification reactions from original DNA.
Immunohistochemistry.
Tumor tissues were fixed in 10% neutral buffered formalin, processed routinely, and embedded in paraffin. Localization ofβ -catenin protein expression was investigated using a polyclonal goat anti-β-catenin antibody (Santa Cruz Biotechnology, Santa Cruz, CA) at a dilution of 1:100 on serial 6-μm sections. Slides were deparaffinized and rehydrated through xylene and ethanol washes into 1× Automation buffer (Biomeda Corp., Foster City, CA). Antigen unmasking was accomplished by heating in 200 ml of citrate buffer in a microwave oven at 50% power for 5 min. Following a 1-min break, the cycle was repeated, and the slides were then allowed to cool for 20 min. Endogenous peroxidase activity was blocked with 3% H2O2 for 15 min. After rinsing in 1 × Automation buffer, sections were blocked with 5% normal goat serum for 30 min. The primary β-catenin antibody was then applied to sections for 1 h at room temperature. Nonimmune rabbit IgG (Jackson ImmunoResearch Laboratories, West Grove, PA) was used as the negative control at equivalent conditions in place of the primary antibody. The bound primary antibody was visualized by streptavidin-biotin-peroxidase detection using the goat Immunocruz staining system (Santa Cruz Biotechnology), according to the manufacturer's instructions, and with 3,3′-diaminobenzidine as the color-developing reagent. Slides were counterstained with Harris hematoxylin, dehydrated through a graded series of ethanol washes to xylene, and coverslipped with Permount (Fisher, Springfield, NJ).
Western Analysis for β-Catenin Protein Expression.
A small number (5) of frozen tumor samples containing hepatoblastomas from the anthraquinone study were obtained for this study. The samples were sectioned with a cryostat, and a single section was quick stained to identify the hepatoblastomas. Then, the unstained hepatoblastomas were dissected away from the rest of the liver tumor and normal tissue to isolate protein. Frozen samples of normal liver, hepatocellular adenomas, and carcinomas from this study were used for comparison. Cellular protein was extracted from these samples for Western blot analysis of protein expression, as described previously (13) .
Mutation Analysis.
A high incidence of malignant hepatoblastomas resulted from anthraquinone or oxazepam treatment of B6C3F1 mice, whereas this tumor type is found only rarely in control mice. In this study, we examined hepatoblastomas induced by these two chemicals for mutations in exon 2 (corresponds to exon 3 in humans) of the β-catenin gene. Mutations were identified in all 19 anthraquinone-induced hepatoblastomas and all 8 oxazepam-induced hepatoblastomas examined (Table 1 ⇓ and Fig. 1 ⇓ , A and B). Multiple point mutations and/or deletions in exon 2 were detected in many hepatoblastomas from both chemical treatment groups.
β-catenin mutation identification in hepatoblastomas and normal liver from B6C3F1 mice treated with anthraquinone. A, SSCP analysis. Shown is a 6% acrylamide/10% glycerol gel with samples amplified with primers 1F × 8R. Lanes 1–8, DNA samples from anthraquinone-induced hepatoblastomas, as shown in Table 1 ⇓ : tumor samples 3, 4a, 7, 9, 11, 19a, 19b (a and b represent different parts of the same tumor), and 6; Lane 9, no DNA control; Lane 10, normal control B6C3F1 mouse liver DNA; Lanes 11–15, DNA samples from five different normal livers from the high-dose anthraquinone group of mice. B, cycle sequencing of β-catenin within exon 2 in four tumor samples. The arrows point to mutations. Sequence 1, hepatoblastoma 4a with deletion of codons 31–38; sequence 2, hepatoblastoma 4b (different part of the same tumor) with mutation at codon 32, GAT to AAT (Asp to Asn); sequence 3, hepatoblastoma 12 with mutation at codon 33, TCT to TTT (Ser to Phe; a different smaller PCR product of this sample had a deletion mutation of codons 5–7, data not shown); sequence 4, hepatocellular carcinoma 43 with no mutation.
Summary of β-catenin mutations in hepatoblastomas from B6C3F1 mice treated with anthraquinone or oxazepam
Point mutations of β-catenin were detected in hepatoblastomas at codons 29–45 (Table 1) ⇓ . Three large hepatoblastomas that had been dissected into two or more parts contained more than one point mutation or deletion found in different parts of the tumor. Two small hepatoblastomas had the same mutations in different parts of the tumors. Fourteen of 19 (74%) anthraquinone-induced hepatoblastomas and 7 of 8 (88%) oxazepam-induced hepatoblastomas contained deletions within exon 2 of β-catenin. Approximately half of the deletions detected in tumors from each chemical treatment group started at codon 5, some affecting the splicing site for exon 2. The deletion mutants we identified removed 3–44 amino acids, and some of these included critical residues in the NH2-terminal phosphorylation region necessary for degradation of the β-catenin protein.
Among the point mutations, any of the three bases of the codon could be mutated, and specific patterns of G to A or G to T mutations were not apparent for either chemical treatment. There did not appear to be a chemical signature mutation pattern in that the spectrum of β-catenin mutations did not differ between the hepatoblastomas from the two different chemicals. Moreover, the pattern of point mutations did not differ from those found in hepatocellular neoplasms induced by chronic treatment with other chemicals (13) .
In National Toxicology Program studies, hepatoblastomas are often found within a hepatocellular adenoma or carcinoma. It has been hypothesized that this tumor may represent a more malignant hepatocellular neoplasm. We, therefore, examined six samples from anthraquinone-treated mice in which a hepatocellular adenoma or a hepatocellular carcinoma was microdissected from the same tissue area as a nearby hepatoblastoma. Two of three adenomas and two of three carcinomas had β-catenin mutations in exon 2 as compared with nearby hepatoblastomas that all had mutations. However, all of the point mutations or deletions in the hepatoblastomas were different from those found in the corresponding hepatocellular neoplasms (data not shown). These results suggested that mutations found in hepatoblastomas may be different and lead to a more malignant phenotype than those in the hepatocellular tumors.
To further address this question, we examined DNA from 63 frozen hepatocellular neoplasms for mutations in β-catenin. Ten of 32 adenomas (31%) and 13 of 31 carcinomas (42%) exhibited β-catenin mutations (Table 2 ⇓ ). Although there were more deletions and more multiple mutations in the hepatoblastomas than in the hepatocellular neoplasms, the spectrum of mutations was not extensively different among the different tumor histotypes. We also analyzed six normal liver tissue samples from mice in the high-dose anthraquinone group and found no mutations in these samples (Fig. 1 ⇓ ). The frequency of mutations in the hepatoblastomas (27 of 27) is statistically higher (P < 0.0001 by Fisher's exact test) than in hepatocellular neoplasms (23 of 63 anthraquinone induced and 18 of 41 oxazepam induced (4) , providing evidence that hepatoblastomas evolve from preexisting hepatocellular neoplasms with β-catenin mutations.
Summary of β-catenin mutations in hepatocellular neoplasms from B6C3F1 mice treated with anthraquinone
Protein Expression.
In addition to mutation analysis, protein expression was performed on a subset of the samples from the anthraquinone study. We evaluated five microdissected hepatoblastomas from frozen samples and eight hepatocellular neoplasms for β-catenin protein expression by Western blotting. In general, the tumors expressed similar or slightly greater levels of the mutant normal-sized or truncated β-catenin protein than was observed for normal liver (Fig. 2 ⇓ ). That we did not observe significantly greater expression in the hepatocellular neoplasms and hepatoblastomas may be due to heterogeneous accumulation of protein in parts of the tumors and/or contamination with normal tissue relative to β-catenin protein.
Expression of β-catenin protein in anthraquinone-induced mouse liver tumors by Western blot analysis. Equivalent amounts of protein from total homogenates of each sample were electrophoresed and immunoblotted, as described in "Materials and Methods." The blot was cut horizontally and developed with anti-β-catenin (top) and anti-actin (bottom). Lane 1, normal liver; Lanes 2–6, hepatocellular neoplasms; Lanes 7–11, hepatoblastomas 2, 5, 13, 6, and 14a.
To examine the intracellular localization of β-catenin in the tumors, we also evaluated some of the samples including seven hepatoblastomas by immunohistochemistry. Immunohistochemical staining of the hepatoblastomas revealed strong membrane, cytoplasmic, and nuclear reactivity (Fig. 3 ⇓ ). This was in striking contrast to normal liver and hepatocellular adenomas and carcinomas from the same sections, in which only membrane staining was observed (Fig. 3 ⇓ ).
Immunohistochemical analysis of β-catenin expression in anthraquinone-induced hepatoblastomas and surrounding liver tumors and tissue. A, hepatoblastoma 14b (not analyzed forβ -catenin mutations) within a hepatocellular carcinoma; H&E (×40). B, the same hepatoblastoma reacted withβ -catenin antibody (×40). Note marked membrane and cytoplasmic staining, compared with surrounding hepatocellular cells of carcinoma with only weaker membrane staining. C, higher magnification of hepatoblastoma in B (×132). D, hepatoblastoma 2 with strong nuclear and cytoplasmic staining (×50). E, high magnification of area in hepatoblastoma showing some cytoplasmic and nuclear staining (×100). F, high magnification of hepatoblastoma showing marked nuclear staining (×200).
β-catenin is a central and critical component of the Wnt signaling pathway (17) and is up-regulated in many human cancers following mutation of either the APC gene or the β-catenin gene (10 , 12) . The striking finding of somatic mutations of the β-catenin gene in all mouse hepatoblastomas induced by anthraquinone and oxazepam is important because these are the same mutations that have been observed in human childhood hepatoblastomas (7) and adult hepatocellular carcinomas (12) , as well as in chemically induced rodent hepatocellular neoplasms (13 , 14 , 18) . The high frequency of β-catenin mutations and accumulation of β-catenin protein in the mouse liver tumors is consistent also with findings in human colon tumors (10) , suggesting that up-regulation of the Wnt signaling pathway is an important step in their pathogenesis. Thus, the occurrence of chemically induced hepatoblastoma formation in the B6C3F1 mouse and its associated molecular alterations seem to be relevant to the human carcinogenic process in liver.
To date, the pathogenesis of hepatoblastomas in mice has not been well defined. Hepatoblastomas occur only rarely in untreated mice of certain strains or following treatment only with tumor initiators such as N-nitrosodiethylamine (19) . However, following chronic treatment of B6C3F1 mice with promoters such as phenobarbital, a high incidence of hepatoblastomas has been observed (20 , 21) . Hepatoblastomas are usually observed within hepatocellular carcinomas and may evolve as a variant or more malignant form of adenoma or carcinoma (3 , 21) . The finding of 31% of anthraquinone-induced adenomas, 42% of carcinomas, and 100% of hepatoblastomas with β-catenin mutations suggests that this molecular event may be critical for the development of hepatoblastomas within existing benign and malignant hepatocellular neoplasms. Previously, we showed that hepatocellular neoplasms in untreated mice have only a low frequency of β-catenin mutations (13) . Thus, the accumulation of β-catenin protein at the cell membrane in the chemically induced hepatocellular neoplasms with subsequent translocation to the nucleus, and leading ultimately to transactivation of growth promoting genes, may provide the oncogenic potential to develop into hepatoblastomas.
We first hypothesized that the β-catenin mutations in the malignant hepatoblastomas would be different from and/or more severe than those in the hepatocellular neoplasms, thus leading to the different phenotype. However, whereas the hepatoblastomas sometimes had multiple β-catenin mutations and many of these were deletions, most of the specific mutations were found in each of the tumor types. Moreover, it could be argued that because of the high incidence of spontaneous hepatocellular neoplasms that lack β-catenin mutations, some of which are found among the tumors in the treated mice, the frequency of β-catenin mutations in the chemically induced hepatocellular neoplasms is actually higher than that observed. These findings suggest that another molecular event is needed for the development of the hepatoblastoma histotype or that multiple mutations lead to a different or more severe phenotype. E-cadherin at the cell membrane and the APC protein in the cytoplasm are known to compete for β-catenin binding (22) . The accumulation of β-catenin along the cell membranes in the hepatocellular neoplasms suggests that at least some β-catenin mutations lead to binding of mutant β-catenin to E-cadherin. It is possible that most of the β-catenin point mutations and some of the deletions in these hepatocellular tumors lead to decreased binding efficiency of APC but not E-cadherin. In contrast, the hepatoblastomas had prominent cytoplasmic and nuclear localization of the β-catenin protein, suggesting that E-cadherin expression may be decreased in these tumors. E-cadherin is a putative tumor suppressor protein for some human cancers (23) and is lost during progression in several human tumor types (24 , 25) . However, another possibility is that some β-catenin mutations (especially larger deletions) alter or remove E-cadherin binding sites from the protein. This could permit unbound truncated, but potentially still active β-catenin protein to move from the cell membrane into the cytoplasm and nucleus. Ultimately, following the binding of cotranscription factors such as Tcf-4 to the mutant β-catenin protein and transactivation of genes such as c-Myc (11) , this cascade of events may result in enhanced cell proliferation. Most studies on human tumors that contain β-catenin mutations have demonstrated cytoplasmic and nuclear staining of β-catenin protein (12 , 26 , 27) , and the mouse hepatoblastomas seem to follow this pattern.
The dominant nature and high frequency of β-catenin mutations identified in the mouse hepatoblastomas in this study suggest that alteration in the stability and regulation of β-catenin expression is an important event in the formation of these tumors in the B6C3F1 mouse. Moreover, the β-catenin mutations are the same as those found in human hepatoblastomas, suggesting that similar carcinogenic pathways exist in the two species. Studies in our laboratory are now investigating the consequences of β-catenin protein accumulation and interaction with other proteins in the development of hepatocellular neoplasms and hepatoblastomas to further understand the mechanisms of chemical induction of liver carcinogenesis in this model.
We thank Drs. David Malarkey and James R. Hailey for critical reading of the manuscript and helpful comments.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
↵To whom requests for reprints should be addressed, at MD D4-04, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, NC 27709. Phone: (919) 541-3241; Fax: (919) 541-7784; devereux@niehs.nih.gov.
↵The abbreviations used are: APC, adenomatous polyposis coli; SSCP, single-strand conformational polymorphism.
Received September 3, 1999.
Accepted April 4, 2000.
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Germany's Response to the Ukraine Crisis | Ambassador John Kornblum
« Russia's Threat to Ukraine: The West Responds | Ambassador John Kornblum
Russia's Threat to Ukraine: The Crisis Unfolds | Ambassador John Kornblum »
Thank you for your continuing support in 2022!
The Tennessee World Affairs Council
in association with the
American Council on Germany
and Belmont University Center for International Business, and the Nashville Area Chamber of Commerce
GLOBAL TOWN HALL
Germany's Response to the Ukraine Crisis
Ambassador John Kornblum
Former U.S. Ambassador to Germany and Assistant Secretary of State for European Affairs
February 1, 2022 @ 10:00 a.m. CT
Dr. Liana Fix
Resident Fellow at the German Marshall Fund Washington office
And Moderator
Dr. Steven E. Sokol
President, American Council on Germany
This special event is free but please consider becoming a member or making a donation when you register. Thank you.
Russia's Threat to Ukraine: Germany's Response to the Ukraine Crisis | Ambassador John Kornblum

When President Joe Biden met the press on January 19th he was candid when addressing consequences for Russia if it attacked Ukraine. "It depends on what [Putin] does as to what extent we're going to be able to get total unity on the NATO front." The White House quickly cleaned up what he "meant" to say. In the days since official statements continue to stress NATO solidarity but questions remain.
For example British aircraft carrying weapons to Ukraine flew "around" Germany sparking media questions about Berlin being onboard for support to Kiev, despite Defense Ministry denials it restricted the flights. That was followed by the resignation of Germany's Navy chief over controversial remarks about the threat to Ukraine. Writing for the Center for European Policy Analysis, Oxana Schmies spoke of "Germany's paralyzing fear of war," and warned that for the new government it was "worryingly clear that forging a united Russia policy is difficult and marred by underlying disagreement. [Link]
As the prospects of Russian provocation and action against Ukraine reach the boiling point it's a fair question to ask where Germany "is," as the United States and allies lean forward in deterrence and preparation for response.
To address this question we turn to Ambassador John Kornblum, preeminent authority on America's relationship with Europe, and Germany in particular.
Ambassador John C. Kornblum has a long record of service in the United States and Europe both as a diplomat and as a businessman. He is recognized as an eminent expert on U.S.-European political and economic relations, in particular in Central and Eastern Europe. He served as the U.S. Ambassador to Germany from 1997 to 2001. Before that, he occupied a number of high-level diplomatic posts, including U.S. Assistant Secretary of State for European affairs, Special Envoy for the Dayton Peace Process, U.S. Ambassador to the Organization for Security and Cooperation in Europe (Helsinki Process), Deputy U.S. Ambassador to NATO, and U.S. minister and deputy commandant of forces in divided Berlin.
The conversation will be guided by the President of the American Council on Germany, Steven Sokol.
Send your questions for Ambassador Kornblum to Questions@TNWAC.org
You can view Ambassador Kornblum's January 17th TNWAC conversation about the Ukraine crisis on our YouTube channel and you can read the transcript.
Ambassador John C. Kornblum has a long record of service in the United States and Europe both as a diplomat and as a businessman. He is recognized as an eminent expert on U.S.-European political and economic relations, in particular in Central and Eastern Europe. He served as the U.S. Ambassador to Germany from 1997 to 2001. Before that, he occupied a number of high-level diplomatic posts, including U.S. Assistant Secretary of State for European affairs, Special Envoy for the Dayton Peace Process, U.S. Ambassador to the Organization for Security and Cooperation in Europe (Helsinki Process), Deputy U.S. Ambassador to NATO, and U.S. minister and deputy commandant of forces in divided Berlin. From 2001 to 2009, he was chairman of Lazard Freres Germany. He currently serves as senior counsellor to the international law firm Noerr LLP and as a senior adviser to the worldwide consultancy Accenture. Mr. Kornblum has also served on a number of supervisory and advisory boards including those of Thyssen-Krupp, Technologies AG, Bayer AG, Russell Reynolds, and Motorola Europe. He is a member of the boards of the American Chamber of Commerce in Germany, the American Academy in Berlin, the Deutsche Oper in Berlin, and of numerous nonprofit organizations on both sides of the Atlantic. He received a B.A. from Michigan State University in 1964, and he has been the recipient of many awards, including a Knights Cross of the Order of Merit from Germany and an Order of Merit from Austria.
Dr. Liana Fix is a Resident Fellow at the German Marshall Fund's Washington office, while on sabbatical from the International Affairs Department of the Körber Foundation in Berlin. She is a political scientist and historian, and her work focuses on Russia and Eastern Europe, European security, arms control, and German foreign policy. She will be focusing on transatlantic policy toward Russia while at GMF. Dr. Fix has published widely in academia, thinktanks, and national and international media. She holds a doctorate degree from the Justus Liebig University Giessen and a master's degree from the London School of Economics and Political Science.
Steven E. Sokol is the President of the American Council on Germany. Previously, he served as President and CEO of the World Affairs Council of Pittsburgh and prior to that he was the Vice President and Director of Programs at the American Council on Germany. Earlier in his career, Steve served as the Deputy Director of the Aspen Institute Berlin, was the Head of the Project Management Department at the Bonn International Center for Conversion GmbH (BICC), and a Program Officer in the Berlin office of the German Marshall Fund of the United States. He holds a Doctorate in Law and Policy from Northeastern University as well as an M.A. in International Relations and International Economics from the Johns Hopkins University's Paul Nitze School of Advanced International Studies (SAIS) and a B.A. from Wesleyan University. He has also studied at the Ruprecht-Karls-Universität in Heidelberg and as a Fulbright Scholar at the Freie Universität in Berlin.
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redpajama_set_name: RedPajamaCommonCrawl


SAN FRANCISCO & ANNAPOLIS, Md.--(BUSINESS WIRE)--Thayer Lodging Group, a value-added hotel investment company, and Quest Hospitality Ventures, a venture capital firm investing in hospitality technology companies, today announced that they have affiliated to form a private equity sponsor, Thayer Ventures, which will be the successor of Quest Hospitality Ventures. Thayer Ventures will focus on sponsoring investment funds, which will invest in emerging technology companies in the global hospitality industry. Now part of Thayer Lodging Group's family of funds, Thayer Ventures will continue to be managed by the four principals of Quest Hospitality Ventures and will fund innovative technology startups in the $10 trillion global hospitality industry.
Thayer Ventures expects to begin making investments in 2013 from its new investment vehicles.
Thayer Ventures will be based in San Francisco and managed by general partners Mark Farrell, Chris Hemmeter and Lucien Ruby – the original founders and managing directors of Quest Hospitality Ventures – and general partner Jeff Jackson, former CFO of Sabre Holdings. Leland Pillsbury, Fredrick V. Malek, Bruce Wiles and George Dabney, each managing principals of Thayer Lodging Group, will serve as senior advisors to Thayer Ventures and its sponsored funds. As the only venture capital fund focused entirely on the hospitality industry, Thayer Ventures has deep knowledge and unrivaled relationships that will allow it to provide unequaled value to technology entrepreneurs.
Along with approximately 75 other limited partners from the hospitality industry, the principals of Thayer Lodging Group seeded Quest Hospitality Ventures' inaugural venture capital fund, which has made investments in eight technology companies in the hospitality industry, including Hipmunk, newBrandAnalytics, Nor1, and Adara Media. Based on the success of this inaugural fund, Thayer Lodging Group and Quest Hospitality Ventures formalized their partnership to create Thayer Ventures. The new venture fund endorses the original investment thesis behind Quest Hospitality Ventures and completes Thayer Lodging's vision to create a global family of hospitality and travel funds across multiple asset classes.
Thayer Lodging Group, based in Annapolis, Md., is a privately held hotel investment company that was formed in 1991 by Frederic V. Malek and Leland Pillsbury. Since its founding, Thayer has established a consistently successful track record spanning every investment cycle. Thayer has invested in more than 100 hotels, and in 2010 acquired Interstate Hotels and Resorts, the world's largest third-party, independent hotel manager, which operates nearly 400 hotels globally. Thayer principals also have numerous investments in hospitality and travel-related companies, including Quest Hospitality Fund I. For more information about Thayer, visit the company's web site, www.thayerlodging.com.
Quest Hospitality Ventures is the only venture capital firm specifically focused on the hospitality industry. Since its founding in 2009, the company has partnered with entrepreneurs to create, develop and build technology companies that will revolutionize the hospitality industry. Based in San Francisco, QHV has backed some of the world's leading travel technology companies, including Hipmunk, hotelme.com, Nor1, Adara Media, Duetto Research, newBrandAnalytics, and ID90T. Additional information is available on the company's website: www.thayerventures.com.
Thayer Lodging Group and Quest Hospitality Ventures affiliate to form private equity sponsor, Thayer Ventures, which will focus on sponsoring investment funds to invest in technology companies.


text:
Apollo Awards 2019
Rakewell
Art News Daily
Apollo Events
UNESCO Reports 'Industrial Scale Looting' in Syria
Our daily round-up of news from the art world
Archaeological Sites Being Looted on 'Industrial' Scale, says UNESCO | Irina Bokova, the director of UNESCO, has stated that world heritage sites in Syria are being looted on an 'industrial' scale by ISIS. According to Bokova, satellite images suggest that archaeological sites across the country are 'dotted by thousands of illegal excavations'. The statement follows an archaeologist's claim that items looted from Palmyra are 'already on sale in London', as reported by Robert Fisk.
Unsuccessful Restitution Claim for Bristol Museum's Renoir | The Bristol Museum & Art Gallery is to stay in possession of a Renoir painting once thought to have been forcibly sold under pressure from the Nazis, reports The Art Newspaper. The Spoliation Advisory Panel's report stated that there was 'insufficient evidence' for the painting to be returned to the descendants of its original owner. A collective sigh of relief emanates from the West Country.
Artes Mundi Prize Shortlist Revealed | Seven artists including John Akomfrah OBE and Neïl Beloufa have been named on the shortlist for the 7th Artes Mundi Prize. Even if it lacks the glamour of the Turner Prize, the Artes Mundi is the UK's biggest award for contemporary art, with the official winner receiving £40,000. Place your bets now…
Tour Montparnasse to Receive €800 million Refurbishment | Loathed it may be, but central Paris's sole skyscraper is to undergo a comprehensive makeover that may cost up to €700 million – less than two years after a politician advocated tearing the building down. Paris mayor Anne Hidalgo hopes the renovation will turn the area into 'the Times Square of Paris'. High hopes indeed.
Detroit Institute of Arts Names New Director | Salvador Salort-Pons has been named as the new director of the Detroit Institute of Arts. Madrid-born Salort-Pons, who is currently executive director of collection strategies and information, has been at the Institute since 2011.
Salvo (1947–2015) 'È Morto' | The Italian artist Salvatore Mangione, better known as 'Salvo', has died aged 68. Salvo, who was known for placing himself at the centre of his work, left behind a typically self-referential epitaph, reading 'SALVO È MORTO' ('Salvo is dead'). The phrase was carved on the reverse of a 1973 marble sculpture inscribed with the phrase 'SALVO È VIVO'.
There's never been a better time to subscribe to Apollo magazine. Start your subscription now.
More art news
Artes Mundi: the director's tour
As we wait to hear the winner of this year's prize, director Karen MacKinnon discusses the shortlisted works and what they mean to her
What happens if you unwittingly buy a looted artefact?
We ask a legal expert for their advice to concerned collectors
The Spoliation Advisory Panel and Art Restitution Claims
Items from the Tate, V&A and Ashmolean museum are being investigated by the Spoliation Advisory Panel: what is the panel, and what do they do?
Follow us Like us Follow us Subscribe
A legal guide to the new anti-money laundering rules in the UK
The 5th Anti-Money Laundering Directive has passed into UK law. What impact will it have on the British art market?
The Kariye Museum in Istanbul – a Byzantine masterpiece under threat
A court recently ruled that the ancient site be reconverted into a mosque, casting the fate of its well-preserved mosaics and wall paintings into question
google_a
The ace caff that now leaves a bad taste – at the V&A Café
Thomas Marks
Food for thought – the art of the museum restaurant
May Morris was a master of many crafts, but it's her embroideries that steal the show at Dovecot Studios
Robyne Calvert
The Victorian collectors who loved art from ancient Egypt
Leonardo at the Louvre is full of wonders – and a few surprises
Charles Nicholl
Roberto Cicutto named president of Venice Biennale
Hester Diamond (1928–2020)
What did Venice look like to a medieval pilgrim from Tuscany?
Deborah Howard
The private collection that paved the way for the National Gallery
Hong Kong shuts public museums as a result of the coronavirus
The Apollo 40 under 40 podcast: Mahmoud Khaled
The artist talks to Gabrielle Schwarz about how an upbringing in Egypt has shaped his work exploring gender, queer desire, politics and power
Apollo's art diary
Gods in Color
The acclaimed touring exhibition of classical polychromy returns to Frankfurt in expanded form
Sahel: Art and Empires on the Shores of the Sahara
Sculptures, textiles and manuscripts tell the story of civilisation across the vast region in Africa
Luminous Figures
Shining new light on the popular genre of stained-glass painting in 16th-century Switzerland
Wilhelm Leibl – The Art of Seeing
The German painter's clear-eyed realism brought him to the attention of Courbet – and had a strong influence on Van Gogh
A 14th-century sketch by a travelling friar is now thought to be the earliest known drawing of the city
From casual cafes to fine dining – the eating options at a museum can tell us a great deal about how it sees itself
Could contemporary art be less wasteful?
What effect do contemporary artists have on the environment – and should this affect what we think about their work?
About Apollo
© 2020 Apollo Magazine
22 Old Queen Street, London, SW1H 9HP


It is not rude, it is not self-seeking, it is not easily angered, it keeps no record of wrongs. Love does not delight in evil but rejoices with the truth. It always protects, always trusts, always hopes, always perseveres. Love never fails. But where there are prophecies, they will cease; where there are tongues, they will be stilled; where there is knowledge, it will pass away.
For just as the body is one and has many members, and all the members of the body, though many, are one body, so it is with Christ. For kin one Spirit we were all baptized into one body—Jews or Greeks, slaves or free—and all were made to drink of one Spirit.
Preaching is NOT a cooking show! When people are hungry they don't want the recipe they want a meal. Please come have that meal with us.
I'm humbled and excited about this journey. My vision for New Direction is to lead God's people by example, into righteous living, tithe giving, and worshipping. God's word alone is my guide. To preach and teach the Gospel in such a manner that it reaches the youngest to the oldest, draws the greatest of sinners and challenges each of us to trust and obey God and His word. To develop and implement ministries that will train men and women into their God given positions and purposes.


text:
Jordyn Woods Is Having a Hot Girl Summer
The controversial figure just posted a series of photos with the patron saint of Hot Girls, Megan Thee Stallion.
by Brooke Kushwaha
c/o BET
If Jordyn Woods is pressed about missing former bestie Kylie Jenner's birthday party, she isn't showing it. The former reality personality turned it-girl recently spent time with resident Hot Girl Megan Thee Stallion, posting enviable pics on Twitter and Instagram with the caption, "real hot girl shit." The hangout comes right after a weekend of Jenner celebrating her 22nd birthday in Capri, Italy, where the cosmetics mogul reportedly rented a $250 million yacht for her close friends and family (of which, Woods is no longer part).
Despite having opened up about her cheating scandal on multiple occasions, Woods has stayed relatively unbothered in the aftermath of the drama. Posing with Megan Thee Stallion, this moment's it-girl and the originator of the phrase "Hot Girl Summer," classifies as a baller move in all respects. Since her rise to fame, Thee Stallion has preached self-love, career moves, and sexual liberation all in the name of being a Hot Girl—and as she's proven with comments on the matter, everyone's included. Meg also recently spent time with fellow musician Lizzo, during which the "Juice" singer's iconic flute made a cameo as the two took shots and generally participated in carefree revelry.
The 10 Cutest Curly Hair Trends for 2021
Since its posting on Monday night, Woods' photo op with Hot Girl Meg has amassed over a million likes on Instagram as well as thousands of retweets. When you think about it, Megan Thee Stallion is the perfect partner in crime for Woods, who has faced public shame and ridicule surrounding the murky details of her involvement with Khloe Kardashian's husband Tristan Thompson. Although some have accused the star of opportunism following the scandal, you could also argue she's just trying to make the best out of a bad situation.
Megan Thee Stallion, meanwhile, has set herself apart from many of her rap contemporaries for her commitment to supporting, not beefing with, her fellow musicians. She recently collaborated with Nicki Minaj and Ty Dolla $ign on the long-awaited single "Hot Girl Summer" and has been teasing several other collabs in the works. Although we aren't sure if Woods would hop onto a track, partnering with Meg is a statement of unapologetic self-ownership. Meg recently spoke on how she plans to extend Hot Girl Summer into the fall and winter months, giving the blueprint for a Hot Girl attitude. Looks like even though it's about to be a sad girl fall, it just might be a hot one too.
"You cannot worry about other people's opinions," the affirming rapper told Access Hollywood. "You gotta love yourself. You wake up with yourself. You go to sleep with yourself. You should be the only person you're trying to please."
Stallion's words are key to living the Hot Girl Lifestyle, as the up-and-coming rapper puts it, but they also seem perfectly tailored to Woods' situation. Even in the glaring public eye, Woods ultimately has to become comfortable with herself and her actions, which is no easy feat when you have America's arguably most powerful family blacklisting you left and right. Kylie was the last of the Kardashian-Jenner clan to unfollow Woods on social media, after she again got in hot water by partying with Khloe's ex James Harden. Even as Woods gains magazine covers and sponsorship deals, she's still lost a large part of her support system. If she feels any guilt for her role in Thompson's cheating (because, let's be honest, it's mostly his fault, anyway) then she's also hurting internally.
The Kardashians have been eager to turn Woods into a media pariah, but instead of accepting her scarlet letter, the star has dared to capitalize on the outrage. And when you really think about it, what Kardashian could blame her for that? Perhaps they're furious she's beaten them at their own game, using a bit of tabloid shame as fuel for an empire. If you needed any reminder behind the spray tans and plastic surgery that the Kardashian-Jenner sisters are still white, you need look no further than their victim complex. Woods is making new friends in high places, and she doesn't need Kylie's jet for that. Whether she will ride this fame beyond her fifteen minutes is currently unclear, but for now, she's inarguably having a summer to remember.
c/o @jordynwoods
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Politics & Culture


text:
from idbase.util import localized_datetime_string_now, datetime_diff_seconds
from mock import patch
import re

def test_localized_datetime_string_now_pacific_time(settings):
    settings.TIME_ZONE = 'America/Los_Angeles'
    local_time = localized_datetime_string_now()
    assert local_time.endswith('-07:00') or local_time.endswith('-08:00')

def test_localized_datetime_string_now_no_microseconds(settings):
    """
    Test that our datetime doesn't have microsecond precision, which IRWS
    doesn't have space for.
    """
    settings.TIME_ZONE = 'America/Los_Angeles'
    local_time = localized_datetime_string_now()
    assert re.match(r'\d{4}-\d{2}-\d{2}T\d{2}:\d{2}:\d{2}-0[78]:00',
                    local_time)

def test_datetime_diff_seconds_one_hour():
    assert datetime_diff_seconds('2015-10-15T12:07:07.055934-07:00',
                                 '2015-10-15T13:07:07.055934-07:00') == 3600

def test_datetime_diff_seconds_naive_older_time():
    assert datetime_diff_seconds(
        '2015-10-15T06:00:00',
        newer_time='2015-10-15T00:00:00.0-07:00') == 3600

def test_datetime_diff_seconds_naive_newer_time():
    assert datetime_diff_seconds(
        '2015-10-15T00:00:00-07:00',
        newer_time='2015-10-15T08:00:00') == 3600

def test_datetime_diff_implicit_now():
    with patch('idbase.util.localized_datetime_string_now') as mock_now:
        mock_now.return_value = '2015-10-15T08:00:00.0-07:00'
        assert datetime_diff_seconds('2015-10-15T07:00:00.0-07:00') == 3600

redpajama_set_name: RedPajamaGithub


The Trial has been organized for the Admissions.
24th Jan to 28th Jan 2018.
Kindly Download the Registration form.
Please ensure that the Required Documents ( see the list below ) are brought to the school during admission.
For all other queries, parents are requested to schedule a meeting with the school coordinator.
TO KNOW MORE DETAILS, CONTACT OUR OFFICE TODAY.


I am a girl, who is very very intrested in law of attraction. I have many experiences in that But my native language is estonian and I'd like to improve my english with girls who are from united states or united kingdom We can speak about LOA and I can teach you estonian if you want.
So, write me or leave here your e-mail maybe?
How can I use LOA to learn English and change my characters ?


text:
PENNSYLVANIA TAXPAYERS CYBER COALITION
Dedicated To Equitable Tax Funding Of Pennsylvania Schools
PTCC Home
contact the ptcc
the ptcc on facebook
The Property Tax Independence Act,
HB 76 and SB 76
HB/SB 76 Explained The HB/SB 76 personal calculator HB/SB 76 faqs why HB/SB 76? Ten Reasons to Eliminate How to respond to Naysayers how can I help?
Other Legislation
HB 1189 (OPTEA) act 1 hb 1600 (expired)
The Pennsylvania Coalition of Taxpayer Associations
pcta member groups | pcta resolutions | pcta press releases
PTCC Action Items | PTCC archive | Find Your Legislators | contact the PTCC |
IMPORTANT! The short and long term impacts of enacting The Property Tax Independence Act. Click here.
A great piece from G. Terry Madonna and Michael Young. RIP: The School Property Tax! Click here.
We need property tax reform now! Speakers cheer on House, Senate bills 76. Click here.
Your home's equity is being stolen! How property taxes are reducing your home's value. Click here.
The brutality of tax eviction! A deputy sheriff speaks out. Click here.
* ACTION ITEM *
The Real Faces of the Issue. Click here.
STAY INFORMED! Please Subscribe to free PTCC e-mail updates. Click here. (pataxpayers@gmail.com)
Personal Property Tax Independence Act Tax Calculator
Excel calculator to see your tax savings under the provisions ofThe Property Tax Independence Act. Now includes calculations for Philadelphia property tax reduction!
The Property Tax Independence Act Petitions
Sign an individual petition to demonstrate your approval of the The Property Tax Independence Act or distribute a multi-signature petition to really gather support! Print extra copies for your friends, family, and neighbors so they can help, too! Download the petitions as PDF files here.
Why school property taxes need to be eliminated!
Two excellent essays on the fallacy of property taxes for education funding.
Defeat House Bill 1600!
Another fraudulent property tax "relief" measure
A printer-friendly version of this page in Adobe Acrobat (PDF) format is available here. To ensure proper printing, please use Acrobat's print icon instead of your browser's "Print" command.
Please note: House Bill 1600 was introduced during the 2007-2008 legislative session and expired in committee with the end of the session on November 30, 2008. It is presented here strictly for historical purposes as an example of the measures taken by some members of the Pennsylvania House of Representatives to deceive voters with the promise of property tax "relief". It is no longer an active bill.
House Bill 1600 has totally changed from its original version!
The original language of one of the bills that the PTCC and PCTA oppose, HB 1600, is DEAD. A gut-and-replace amendment by Rep. John Perzel (R-Philadelphia) that would take ALL gambling proceeds and give them to senior citizens earning less than $40,000 passed on January 29, 2008. It totally replaced the original language in HB 1600, effectively killing the bill. For your reference, a synopsis of the original HB 1600 can be found later on this page.
If this amended bill gets through final passage in the House and is passed by the Senate and signed by the Governor, and since this bill uses ALL of the available gambling proceeds that were originally slated for broad-based property tax reduction, any property tax "relief" from gaming money that you've been expecting for two years will be eliminated if you do not meet the guidelines above. This is good news for low-income seniors who are having problems just staying in their homes and we think that this goes a long way towards helping the most vulnerable group in our society. However, the flip side is that the House has reneged on its promise of property tax relief for ALL homeowners that it made to the taxpayers of Pennsylvania two years ago with Act 1. This is ironic since they could have given elimination to ALL homeowners through HB 1275 but refused to do so.
Further, consider this:
- This bill requires the entire projected $1.2 billion in gambling money to meet the current funding for the identified group of recipients.
- Casino revenues have a finite limit and will eventually flatten over time, with zero to minimal growth.
- Property taxes will continue to rise unabated.
- The largest single generation in US history, the baby boomers, are just now starting to retire and will dramatically increase the number of beneficiaries under this plan during the next ten years.
Considering these facts, this plan simply won't work. Where will the money then come from to fund this plan as property taxes rise and the number of recipients expands? Raise other taxes or reinstate a portion of the property tax for recipients? Many seniors who will initially get the full amount will be very disappointed and financially hurt when the subsidy is reduced as more new recipients come on line.
This proposal has been widely criticized as election-year politics and has been the subject of many negative newspaper editorials throughout the state. The amendment is obviously pandering to the senior vote during an election year, but what really irritates me about the Perzel amendment is that it is more of the same "divide and conquer" strategy. I'm sure that these lawmakers feel that with the passage of this bill the seniors (the biggest voting bloc) will be satisfied and they won't have to deal with the issue any more. If this is true, we'll just have to prove to them that this strategy won't work.
The PTCC and PCTA oppose this new HB 1600 as vigorously as we did the original version.
The original HB 1600 (RIP)
On July 17, 2007, Representatives David Levdansky (D-39, Allegheny/Washington) and Mario Scavello (R-176, Monroe) introduced House Bill 1600, another valueless, fraudulent property tax "relief" measure.
Being advertised as a "good first step" (how many times have we heard THAT?!), HB 1600 is exactly the same as the Act 1 referendum that was resoundingly thrashed at the polls in May, 2007. It imposes a 0.5% increase in the sales tax to 6.5% and a .22% increase in the state income tax to 3.29% in return for an approximate $414 homestead exemption. The legislators who support this bill are telling us that it will offer an average 40%-50% reduction in property taxes, but this is absolutely untrue and is simply more smoke and mirrors to try to gain taxpayer acceptance (and votes in 2008!).
HB 1600 is based on EXACTLY the same principle as the Act 1 tax shift. It imposes new, permanent taxes in exchange for minimal temporary "relief" that will quickly be eaten up by relentlessly rising property taxes. HB 1600 will not only leave taxpayers with their same burdensome property tax bills PLUS additional new taxes, it also will do nothing to address the antiquated, crumbling education finance system, the cost of education, or equitable funding for public schools. It is another valueless Band-Aid approach that will again leave Pennsylvania homeowners without true, effective property tax reform and is actually a tax INCREASE in disguise.
Further, unlike the Act 1 referendum where voters had a voice in rejecting the measure, HB 1600 can be enacted and jammed down our throats with no input whatsoever from taxpayers.
The House Finance Committee held seven dog-and-pony-show hearings on House Bill 1600; they pretty much worked against the sponsors of this useless legislation. The lawmakers who are promoting this measure received mostly negative comments from both taxpayers and those who testified at the hearings, with many of the hearings turning raucous because of loud taxpayer discontent with this old, tired, valueless "solution" to the property tax crisis. On September 6 the Reading Eagle hammered the Committee in a scathing editorial because the Committee turned deaf ears to the taxpayers' wishes.
I am astonished at the arrogance of these legislators who think that they can again ignore the taxpayers while they regurgitate the same old plan that has failed three times in the past and still expect us to fall for their charade. Their utter disregard for the intelligence of Pennsylvania taxpayers is incomprehensible and they must be told unequivocally that we WILL NOT tolerate any more of their misguided halfway measures.
It is notable that a number of the original co-sponsors of HB 1600 withdrew their co-sponsorship of this bill after realizing that the measure is valueless. We send our heartfelt thanks to these representatives for the courage and integrity they exhibited by doing this.
The most pressing concern with HB 1600 is that if it is enacted the legislature will tell us that they have given us property tax relief and nothing more will be done for the foreseeable future. As much as they like to tell us that this is another "first step", we know that if HB 1600 passes it will be the LAST step towards true education finance reform for a very long time.
We MUST fight this measure in any way possible.
Please call, write, or e-mail your district's Representative to let them know that you do not want HB 1600 in any manner whatsoever and that you will hold them accountable in the 2008 elections if they support this bill. Further, let them know that you DO NOT CARE if a statewide tax such as the sales tax is raised as long as it ELIMINATES school property taxes. We must get these messages to the legislators NOW!
If you do not know your Representative's contact information it is available by Zip+4 here.
NEW! Calculate your taxes under the School Property Tax Elimination Act. Click here.
Please subscribe to the PTCC e-mail newsletter to receive up-to-date information about the School Property Tax Elimination Act and suggestions for what you can do to help achieve its enactment. Click here.
© 2016 PTCC | Design by Andreas Viklund


text:
import { YError } from '../yerror.js';
let previouslyVisitedConfigs = [];
let shim;
export function applyExtends(config, cwd, mergeExtends, _shim) {
    shim = _shim;
    let defaultConfig = {};
    if (Object.prototype.hasOwnProperty.call(config, 'extends')) {
        if (typeof config.extends !== 'string')
            return defaultConfig;
        const isPath = /\.json|\..*rc$/.test(config.extends);
        let pathToDefault = null;
        if (!isPath) {
            try {
                pathToDefault = require.resolve(config.extends);
            }
            catch (err) {
            }
        }
        else {
            pathToDefault = getPathToDefaultConfig(cwd, config.extends);
        }
        if (!pathToDefault && !isPath)
            return config;
        if (!pathToDefault)
            throw new YError(`Unable to find extended config '${config.extends}' in '${cwd}'.`);
        checkForCircularExtends(pathToDefault);
        previouslyVisitedConfigs.push(pathToDefault);
        defaultConfig = isPath ? JSON.parse(shim.readFileSync(pathToDefault, 'utf8')) : require(config.extends);
        delete config.extends;
        defaultConfig = applyExtends(defaultConfig, shim.path.dirname(pathToDefault), mergeExtends, shim);
    }
    previouslyVisitedConfigs = [];
    return mergeExtends ? mergeDeep(defaultConfig, config) : Object.assign({}, defaultConfig, config);
}
function checkForCircularExtends(cfgPath) {
    if (previouslyVisitedConfigs.indexOf(cfgPath) > -1) {
        throw new YError(`Circular extended configurations: '${cfgPath}'.`);
    }
}
function getPathToDefaultConfig(cwd, pathToExtend) {
    return shim.path.resolve(cwd, pathToExtend);
}
function mergeDeep(config1, config2) {
    const target = {};
    function isObject(obj) {
        return obj && typeof obj === 'object' && !Array.isArray(obj);
    }
    Object.assign(target, config1);
    for (const key of Object.keys(config2)) {
        if (isObject(config2[key]) && isObject(target[key])) {
            target[key] = mergeDeep(config1[key], config2[key]);
        }
        else {
            target[key] = config2[key];
        }
    }
    return target;
}


text:
Forensics Colleges » Forensic Education Blog » Resources » Top True Crime & Forensics Podcasts (2022)
Top True Crime & Forensics Podcasts (2022)
There are over 18.5 million podcast episodes available on iTunes. In 2021 over 57 percent of the US population listened to a podcast, and over 100 million people listened to a podcast every week. As podcasts continue to proliferate, true crime has seen a huge surge in popularity as a genre.
Academics have pointed to a few different reasons for this. Dr. John Mayer, a psychologist, specializing in violence in media, believes exposure to true crime topics is a way for people to build up a tolerance for something frightening. Social psychologist Dr. Amanda Vicary conducted a study that suggested it had more to do with the alluring psychological content implicit in cases of true crime. A simpler explanation might have to do with the fact that humans are narrative-driven creatures, and true crime tales are some of the most engrossing you can find.
Podcasts like Serial set a new bar for the genre. Suddenly, true crime podcasts weren't just guilty pleasures: they were educational, Peabody-winning stories that could have an impact on precisely the topics that they were exploring. Serial was just the beginning, and countless other true crime and forensics podcasts are just waiting to be discovered. Below, we've picked ten of the best.
In selecting our top true crime and forensic podcasts in 2022, we strove for diversity, quality, and originality. Our list touches on all the main areas of the true crime and forensic podcast map. We have comedic shows, scientific examinations, episodic seasons, and individual vignettes. These podcasts cover the hard forensic sciences, the evolving digital forensics scene, and even the institutional systems which prosecute and sometimes perpetuate injustice.
We didn't just pull the most listened-to podcasts off of the charts, because you've probably already listened to those yourself, but we've still included a few heavy hitters, in case you missed them. After some lengthy (and enjoyable) research, these podcasts are the ones that had us going back for more.
Hopefully, you'll find your new favorite from the list below. We know we did.
Since 2013, Sword and Scale has been tantalizing listeners with the dark side of humanity. They primarily focus on the criminal underworld and the criminal justice system's response to it. These stories are not for the faint of heart and cover the most bizarre forms of crime, such as cannibalism and dismemberment, along with more common ones like rape, murder, and abduction. For example, episode 33 and 34 covers the bizarre story of Luka Magnotta, who posted a video of his murder and dismemberment of international student Jun Lin.
During the first year of the podcast, over 1 million episodes were downloaded. Mike Boudet, the show's host, rounds out each episode with court testimonies, 911 calls, and interviews. Episode after episode delivers a full 360-degree view of the entire story. However, listeners should beware as often these audio clips are truly graphic and horrifying. With eight seasons and over 287 episodes, this podcast is prime binge material.
Recommended Episodes: Luka Magnotta (Ep. 33 and 34)
For fans of Serial, Bear Brook may be one of the few imitators that's worthy of taking up the throne. The Bear Brook murders reference what was once a cold case wrapped inside another cold case, involving bodies found skeletonized inside barrels in a New Hampshire park. Decades later, the podcast, a product of New Hampshire Public Radio, helped push the case forward. Reporter Jason Moon, who produced the show, was himself sucked into the story back in 2015.
In a story that spans several decades, Moon pulls apart the numerous threads at work in the Bear Brook case, particularly concerning forensic science. Several investigators, police officers, and amateurs (many of whom were women), contributed to the case. Forensics experts also played a critical role, as the podcast explored and popularized genetic genealogy, a forensic method that helped break the Golden State Killer case in 2018.
Catch and Kill, from Pulitzer Prize-winner Ronan Farrow, blurs the line between investigative journalism and true crime. It's based on his book, which is, in turn, based on his reporting on Harvey Weinstein, which helped created the #MeToo movement. This goes deeper than the Weinstein trial in New York City. This is the story of a journalist's investigation into a seedy world that includes Ukrainian double agents, Israeli private intelligence, and numerous victims who were brave enough to do the right thing in the face of retribution from nefarious criminal elements.
The podcast, Farrow says, has presented an opportunity to revisit the interviews with those brave sources who helped break a story that led to a social revolution. Drawing on original recordings, the podcast has a visceral yet narrative feel, and it's unfolding at a time when the events it discusses are still unspooling in the news.
Double Loop
If you actually want to educate yourself on the ins and outs of forensic science, there aren't many podcasts that can scratch the itch as well as Double Loop. Hosted by forensic scientists Glenn Langenburg and Eric Ray, the show goes into significant detail about latent prints, bloodstain analysis, and scientific articles related to forensic science. They also do in-depth reviews, from a forensic point of view, of mainstream true crime series such as The Staircase and Making a Murderer.
It may be a little dense for casual listeners, but if you're a true crime fiend who's also interested in the hard forensic sciences, Double Loop should be on your list.
Recommended Episodes: The Staircase (Ep. 175-177)
Crimetown
Part of the successful Gimlet Media network, Crimetown explores how organized crime has shaped different cities. So far, it's looked at Providence and Detroit, and it goes into how individuals and institutions sometimes work together to foster an environment that blurs the line between politics and crime. As one of the interviewees says in season one, when describing a prison fight he initiated: if you want to be bad, you have to be good at it.
Crimetown is produced by Marc Smerling and Zac Stuart-Pointer, the duo responsible for the film Catfish and HBO's The Jinx. But Crimetown itself draws more comparisons to wide-lens podcasts like Serial and Netflix miniseries like Making a Murderer. It's one of those shows where it sounds like fiction, but isn't: it's true crime. And, like the best true crime shows, it redefines who the perpetrators really are.
Recommended Season: Providence (S1)
Darknet Diaries
Where many true crime podcasts could arguably be reclassified as history, Darknet Diaries is firmly rooted in the present. Hosted by Jack Rhysider, this podcast explores true crime on the darknet. Hackers, kingpins, cryptocurrency lords, it's all here. It's easy to mistake Rhysider's voice for Ira Glass of This American Life, but only part of that is due to auditory similarity. The other part concerns how well-researched the show is, and how cleanly its complex elements are explained in a tightly-knitted narrative.
There's little, if any, blood in these tales from the dark side of the internet. But they're firmly rooted in the pulse of the future. Listening to an episode about a darknet drug dealer is akin to taking an intro-level course on onion addresses, PGP encryption, DDoS attacks, and cryptocurrency tumblers; but it feels as engaging as any other story you're likely to find. After listening to Darknet Diaries, many other true crime podcasts begin to seem as if they take place in an era when the world was black and white.
Recommended Episode: The Beirut Bank Job (Ep. 6)
Forensic Transmissions
Forensic Transmissions is absolutely terrifying, and it's like no other true crime podcast. It's a straightforward presentation of the facts, but the sum adds up to far more than the parts. These episodes feature no outside narration, no cogent summary, no musical interludes: they're simply unedited, public domain audio of interviews, monologues, and soundbites about criminal cases. Think of them as collections of evidence.
The art of Forensic Transmissions lies in the quiet curation of its public domain audio. In one episode, the chilling monologues of incel shooter Elliot Rodger in Santa Barbara are set next to police interviews with incel shooter Alek Minassian in Toronto. The terror is in what's being presented, in its purest form. For most of the show, you have the voice of a mentally disturbed murderer in your ear. As a listener, you're left to draw conclusions, make connections, and find your own semblance of closure.
If you are interested in working in a forensic field, this might be the sort of thing you're exposed to in the course of your job. Or, if you have a burning curiosity to listen to what investigators listened to and less interest in hearing other people's regurgitated commentary, then this is the show for you. Just be careful. It can't be overstated how disturbing Forensic Transmissions can be, so listen at your own discretion, and wash your ears out afterward.
While the last episode was published in July of 2021, this podcast still makes the list because of the uniqueness of the content and persistent popularity.
Recommended Episode: Incel Uprising (Ep. 116)
How can you beat that title? Here, researcher Marcus Parks, radio personality Ben Kissel, and comedic actor Henry Zebrowski create an atmosphere that reminds one of three best friends on a starlit camping trip, holding flashlights under their chins as they collectively tell the stories of some of the creepiest, goriest, most fascinating true crime stories. Luckily, those best friends have a few cans of beer, a whole host of conspiracy theories, a killer sense of humor, and a surprising grasp of both history and the occult.
Last Podcast on the Left is one of those podcasts where you're embarrassed if your headphone falls out, because someone might hear what you're listening to, but it's compounded by the fact that, if such an event does happen, you'll probably be laughing, too, despite the horrific reference material.
Over the last six years, the narrators of LPOTL have developed a real camaraderie and a flawless knack for comedic rhythm. Despite the bend towards humor, the episodes are incredibly well researched, so you might learn something while you listen, despite your best efforts.
Recommended Episodes: The Oklahoma City Bombing (Ep. 274-277)
My Favorite Murder
Science suggests that while violent criminals are more likely to be male, true crime fans are more likely to be female. So if you think that the Last Podcast on the Left is a little too much of a boy's club, check out My Favorite Murder, hosted by Karen Kilgariff and Georgia Hardstark. These two comedians, LPOTL fans and true crime aficionados met at a Halloween party and bonded over a story of a lethal car accident, so if that sounds like a context that would draw you in, you've found the right true crime podcast. Karen and Georgia will make you feel a whole lot less alone in your true crime obsession.
It might be a little less factually correct or doggedly researched than other true crime podcasts (some episodes include a segment specifically devoted to correcting their errors in other episodes), but the informal and comedic style makes it easier to stomach and fully binge-able.
Karen and Georgia often say that the podcast is a form of therapy for themselves, a way to deal with their own anxieties. They're not the only ones: with over half a million downloads per episode by loyal fans (who call themselves 'Murderinos'), the podcast has been hailed as a type of mental health support group by The Atlantic. As the podcast's sign-off goes: stay sexy and don't get murdered!
Recommended Episode: My Firstest Murder (Ep. 1)
The Missing Cryptoqueen
Dr. Ruja Ignatova, the subject of The Missing Cryptoqueen and investigation, was the face of a new kind of cryptocurrency before the mainstream public even knew what cryptocurrency was. What she might have lacked in scruples she made up for with charisma and good timing: by 2017, the cryptocurrency market had taken off, and Dr. Ruja's OneCoin project had soared along with it. The only problem was that OneCoin didn't actually have a cryptocurrency, which investors didn't realize until after Dr. Ruja disappeared. Was she murdered, hiding, dead?
In this podcast, the BBC's Jamie Bartlett takes us into the case from the very beginning, breaking much of the story as he reports on it. The show goes beyond the fundamentals of cryptocurrency and susses out the details of what differentiates an opportunity from a crime in this field. All the elements of a compelling story are here: white-collar crime, cult-like leadership, cutting-edge tech, and global scale. It's easy to get caught in the narrative, and, while listening to speeches from Dr. Ruja, you may wonder if you would've been able to avoid the trap, too.
Parcast is a controversial podcast network. Their shows seem almost puritanically dedicated to a stripped-down style. Even the names of their shows—Conspiracy Theories, Cults, or in this case, Serial Killers—get directly to the point. The content is no different: hosts Greg Polcyn and Vanessa Richardson speak in the predictable, occasionally cheesy cadence of late night news reporters. You might sometimes find yourself chuckling and wondering if it's all on purpose. We may never know. It makes the show even more engrossing.
Where the podcast is concerned with detail, though, is where it counts. Polcyn gets into forensic specifics of the crimes, and Richardson gets into psychological analyses of the criminals. Their coverage of Ted Bundy (who had one of the first murder trials to ever be televised) is comprehensive enough to give you a sense of where this true crime craze started, and how, for better or worse, the media exacerbated it.
Recommended Episode: The Campus Killer (Ted Bundy)
Matt Zbrog
Matt Zbrog is a writer and freelancer who has been living abroad since 2016. His nonfiction has been published by Euromaidan Press, Cirrus Gallery, and Our Thursday. Both his writing and his experience abroad are shaped by seeking out alternative lifestyles and counterculture movements, especially in developing nations. You can follow his travels through Eastern Europe and Central Asia on Instagram at @weirdviewmirror. He's recently finished his second novel, and is in no hurry to publish it.
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If you have an undergraduate degree in criminology, psychology, sociology, or history under your belt and you're exploring your options for higher education, you might consider pursuing a master's degree in criminal justice.
National Criminal Justice Month 2021: An Advocacy Toolkit
March is National Criminal Justice Month.
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"Defunding the police" means reallocating some portion of a police budget to community services such as housing, health, counseling, and education.
The Great Capital Punishment Debate: Are Executions of Criminals Ethical?
In 1972, the outcome of Furman vs Georgia put a nationwide moratorium on the practice of capital punishment in the United States.
National Forensic Science Week 2021: An Expert's Advocacy Guide
Both science and justice are, in essence, the pursuit of truth.
Crime Prevention Month: Expert Interview & Advocacy Guide
Benjamin Franklin said that "an ounce of prevention is worth a pound of cure," and this quote remains relevant, particularly regarding crime prevention.


text:
Ragland loves football
Congratulations Class of 2018
Online Green & Gold
Media Academy
Martin Reynolds comes to Fremont
Luz Morales, Staff Reporter|March 2, 2017
Photo by: Jasmene Miranda
Bay Area native Martin Reynolds never planned on being a journalist. He found it by accident when he transferred to Merritt College and signed up for a class called, "Writing for Mass Media." Now he's an investigative journalist that works for the Center for Investigative Reporting promoting diversity in the media.
Reynolds came to Fremont High in December and spoke to students about his path to journalism and his experience working in the media industry.
According to Reynolds, one of the challenges of being a person of color in a very white and male-dominated industry is that he doesn't always feel like he fits in. "Who I was as a person didn't necessarily jive with the organization that I was in or the people that I was around," Reynolds said.
His background as an artist and person of color always made him stand out. Before Reynolds became a journalist, he was a rapper in a hip-hop group called Ho-Flow. "The notion that you can be who you are as a person, you can bring to your work," he said of his transition from artist to journalist. "Being a lyricist and songwriter made me a better storyteller and journalist. In many ways, I saw the world differently, not just professionally."
One of the first stories that Reynolds published as a Merritt reporter was about the San Francisco earthquake in 1989, when the second floor of the Bay Bridge collapsed. He went to the I-80 freeway and wrote an article about it from a first person point of view.
In 2005, Reynolds graduated from the Robert C. Maynard Institute for Journalism Education which focuses on promoting the fair and accurate coverage of communities of color by the media. Reynolds has also worked with San Francisco State University and University of California, Berkeley as a mentor to undergraduate and graduate journalism students.
Reynolds did not just answer questions from students during his Fremont visit. He also asked every student in the classroom where they consumed their news and what interests them.
Some students shared with Reynolds what they plan to do in the future, and he provided them with some valuable feedback. "Don't seek to be successful for the sake of proving others wrong. Seek to be successful because you want to give something," Reynolds said.
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text:
What are the Signs of Falling in Love?
The early stages of a relationship can be incredibly confusing to say the least. You'll probably feel puzzled about your own feelings, whilst wondering what the person you're dating really thinks about you. You may be struggling to decipher your own emotions, not sure if you're actually falling in love or simply attracted to this new person in your life.
Signs you are really falling in love
1. You discuss doing things or going places in the future. You happily talk about going to an event that's three months away, because you know that you'll still be together then. It's a sign that you're confident about the relationship lasting.
2. You no longer think about your ex. Things are going so well in your new relationship that you have no need to think about what's in the past. You've moved on.
3. You'll happily make little sacrifices for them. Whilst you wouldn't ditch your responsibilities for them, you would cancel lunch with your friends to look after them when they're sick.
4. You can be weird around them. If you're comfortable enough to be your most weird self when they're about, it's a good sign that you're falling in love.
5. They're your go-to person. When something good or bad happens and you want to share the news, they are who you go to first.
6. You'd rather stay in with them than go out. One of the biggest signs that you're falling in love is that a night in watching on a movie on the couch with them is more appealing than a night out on the town.
7. All their nasty habits seem cute. When you're falling in love, even there worst habits (chewing on their toe nails, leaving the cap off the toothpaste etc.), all seem adorable!
8. You miss them after a day apart. A sign that you're falling in love is that you miss your significant other after just a day apart. It's a real ache, and one that shows you've fallen hook, line and sinker.
Symptoms of being in love
Are you experiencing butterflies, a pounding heart and loss of appetite, as well as a euphoric high? Then it's possible that these feelings are symptoms of being in love! Being in love can have a dramatic effect on your body, as well as your mind, causing you to act a tiny bit crazy (as well as ridiculously happy). The 'love chemicals' pumping their way through your system can result in all kinds of side effects, including sweaty palms, light-headedness and a feeling of increased energy due to the constant rush of adrenaline. Some of the symptoms of being in love can be unfortunate to say the least, but you'll put up with them all and so much more for that incredible, delicious feeling of being in love.
The moment you finally realise you're falling in love with someone is perhaps the most exciting yet terrifying moment you'll ever experience. Elation, nerves, butterflies, anxiety, and total euphoria all come together, making you wish there was a pause button in life so you could be with them forever as you are right now.
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HomeFinance What Are the Top 10 Precious Metals? Your Complete Guide
What Are the Top 10 Precious Metals? Your Complete Guide
posted on Nov. 10, 2020 at 6:52 am
Are you wondering how to invest in precious metals?
If so, one of the first things you need to know are which metals are the most precious of all. That's why we've put together this list of the top ten precious metals — to find out what they are, simply keep reading, so you'll know what to invest in!
This metal is a cousin of platinum, and is often used as a platinum alloy. It's frequently used in the making of electronics, and has many similar properties to platinum, including durability — it withstands external elements well.
Rhenium boasts the third highest melting point of all elements, and is often used for making turbine engines.
It's quite a dense metal, and is often added to superalloys that are nickel-based, to improve their resistance to heat. It's often a byproduct of copper mining, too.
What is iridium? It's another relation to platinum — it's used in electronics, vehicles and medicine too.
It's only found in South Africa — nowhere else on the planet — and boasts a very high melting point. It also has a nice white sheen, and is incredibly dense.
Palladium is another precious metal, and is often utilized by the automobile industry to reduce emissions, so it's good for the environment. It absorbs hydrogen, and is heat-resistant and malleable too – it's good for making jewellery.
It might not be the rarest metal of all, but gold is undoubtedly a precious metal with some great qualities including flexibility, durability and of course the popularity of the metal in jewellery. If you're wondering exactly what it is, you can find out here.
We've mentioned a couple of close relations, but now we get into platinum itself.
The metal is resistant to corrosion and highly malleable too. It's used for items such as dentist equipment, aircraft and weapons, but is probably most often used in jewellery.
Rhodium has a silver coat and is valued due to its resistance to both corrosion and heat. It's often used in search lights and mirrors, as well as to finish jewellery — you can find rhodium in Russia, South Africa and Canada.
Osimium-187
A dense metal, osimium is similar to iridium and shares a high melting point too. It's ppretty hard and brittle, and is often used in platinum alloys.
Indium is processed through mining zinc, copper and iron-ore.
It's very shiny and malleable too, and turns white in color. One of the softest metals on the planet, it's often used in the semiconductor industry.
The last precious metal in our list, scandium was discovered in Scandinavia in 1879, and is silvery-white in color. It's found in rare-earth and uranium deposits, but only extracted from ores in a few mines across the entire planet.
These are the top ten most precious metals. No longer will you need to wonder "what are precious metals", as they're all here — you can begin investing in precious metals if you'd like to!
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text:
metrics-migration
=================

.. image:: https://travis-ci.org/yunstanford/metrics-migration.svg?branch=master
    :alt: build status
    :target: https://travis-ci.org/yunstanford/metrics-migration

.. image:: https://coveralls.io/repos/github/yunstanford/metrics-migration/badge.svg?branch=master
    :alt: coverage status
    :target: https://coveralls.io/github/yunstanford/metrics-migration?branch=master

a simple tool to help you migrate your graphite metrics

---------------------------
What is metrics-migration ?
---------------------------

metrics-migration a Python3 tool (async io), designed to help graphite users to migrate metrics
in several ways.

* Migrate whole storage directory.
* Migrate specific whisper file (with new metric name).
* Allow schema change during Migration (Provide schema rule).

-------------
Install
-------------

You can install aiographite globally with any Python package manager:

.. code::

    pip3 install metrics-migration

-------------
Dependency
-------------

Whisper on pypi only supports python2, we should download whisper egg from github.

.. code::

    pip3 install https://github.com/graphite-project/whisper/tarball/feature/py3

-------------
Examples
-------------

Let's get started with several examples.

Example 1. A simple example to migrate a directory.

.. code::

    from migration.migration import Migration
    import asyncio

    loop = asyncio.get_event_loop()
    host = "127.0.0.1"
    port = 2003
    directory = '/Users/yunx/Documents/PROJECTS/metrics-migration/examples'

    async def go():
        migration_worker = Migration(directory, host, port, loop=loop)
        await migration_worker.connect_to_graphite()
        await migration_worker.run()
        await migration_worker.close_conn_to_graphite()

    def main():
        loop.run_until_complete(go())
        loop.close()

    if __name__ == '__main__':
        main()

Example 2. Migrate a whipser file with new metric.

.. code::

    from migration.migration import Migration
    import asyncio

    loop = asyncio.get_event_loop()
    host = "127.0.0.1"
    port = 2003
    directory = '/Users/yunx/Documents/PROJECTS/metrics-migration/examples'
    storage_dir = '/Users/yunx/Documents/PROJECTS/metrics-migration'
    metric = "examples.committedPoints"
    new_metric = 'hello.world'

    async def go():
        migration_worker = Migration(directory, host, port, loop=loop, debug=True)
        await migration_worker.connect_to_graphite()
        await migration_worker.send_one_wsp(storage_dir, metric, new_metric)
        await migration_worker.close_conn_to_graphite()

    def main():
        loop.run_until_complete(go())
        loop.close()

    if __name__ == '__main__':
        main()

Example 3. Have Multiple Directories to migrate ?

.. code::

    from migration.migration import Migration
    import asyncio

    loop = asyncio.get_event_loop()
    host = "127.0.0.1"
    port = 2003
    directories_and_prefixes = [
        ('/opt/graphite/metrics-migration/zon1', 'zon1'),
        ('/opt/graphite/metrics-migration/zon2', 'zon2'),
    ]

    async def go():
        migration_worker = Migration(directory, host, port, loop=loop)
        await migration_worker.connect_to_graphite()
        for (directory, prefix) in directories_and_prefixes:
            wait migration_worker.run(directory=directory, prefix=prefix)
        await migration_worker.run()
        await migration_worker.close_conn_to_graphite()

    def main():
        loop.run_until_complete(go())
        loop.close()

    if __name__ == '__main__':
        main()

Example 4. async with context manager

.. code::

    from migration.migration import Migration
    import asyncio

    loop = asyncio.get_event_loop()
    host = "127.0.0.1"
    port = 2003
    directory = '/Users/yunx/Documents/PROJECTS/metrics-migration/examples'

    async def go():
        """
        Use context manager
        """
        async with Migration(directory, host, port, loop=loop, debug=True) as migration_worker:
            await migration_worker.run()

    def main():
        loop.run_until_complete(go())
        loop.close()

    if __name__ == '__main__':
        main()

------------
Development
------------

Run unit tests.

.. code::

    ./uranium test