William Fox was a Hungarian-American motion picture executive, who founded the Fox Film Corporation in 1915 and the Fox West Coast Theatres chain in the 1920s. Although he lost control of his movie businesses in 1930, his name continues to be used in the trademarks of Fox Corporation. Fox was born in Tolcsva and named Vilmos Fuchs, his parents, Michael Fuchs and Hannah Fried, were both Hungarian Jews. The family immigrated to the United States when William was nine months old and settled in New York City, where they had twelve more children, of whom only six survived. Wilhelm once sold candy in Central Park, worked as a newsboy, worked in the fur and garment industry as a youth. In 1900, Fox started his own company. Always more of an entrepreneur than a showman, he concentrated on building theaters. Beginning in 1914, New Jersey-based Fox bought films outright from the Balboa Amusement Producing Company in Long Beach, for distribution to his own theaters and for rental to other theaters across the country.
He formed the Fox Film Corporation on February 1, 1915, with insurance and banking money provided by the McCarter and Usar families of Newark, New Jersey, the small New Jersey investment house of Eisele and King. The company's first film studio was leased in Fort Lee, New Jersey, where many other early film studios were based at the beginning of the 20th century, he now had the capital to expand his production capacity. In 1925–26, Fox purchased the rights to the work of Freeman Harrison Owens, the U. S. rights to the Tri-Ergon system invented by three German inventors, the work of Theodore Case to create the Fox Movietone sound-on-film system, introduced in 1927 with the release of F. W. Murnau's Sunrise. Sound-on-film systems such as Movietone and RCA Photophone soon became the standard, competing sound-on-disc technologies, such as Warner Bros.' Vitaphone, became obsolete. From 1928 to 1964, Fox Movietone News was one of the major newsreel series in the U. S. along with The March of Time and Universal Newsreel.
After the death of Marcus Loew, head of rival studio Metro-Goldwyn-Mayer, in 1927, control of MGM passed to his longtime associate, Nicholas Schenck. Fox saw an opportunity to expand his empire, in 1929, with Schenck's assent, bought the Loew family's MGM holdings, unbeknownst to studio bosses Louis B. Mayer and Irving Thalberg who were outraged, despite their high posts at MGM, they were not shareholders. Mayer used his strong political connections to persuade the Justice Department to sue Fox for violating federal antitrust laws. During this time, in the middle of 1929, Fox was badly hurt in an automobile accident. By the time he recovered, the stock market crash in October of 1929 had wiped out his entire fortune, ending any chance of the Loews-Fox merger going through if the Justice Department had approved it. Fox lost control of his Fox Film Corporation in 1930 during a hostile takeover. In 1935, Fox Film Corporation would merge with 20th Century Pictures, becoming 20th Century-Fox, renamed "20th Century Fox" and, after the 2019 spin-off of Fox Corporation, "20th Century Studios."
William Fox never had any involvement with the film studio. A combination of the stock market crash, Fox's car accident injuries, government antitrust action, forced him into a protracted seven-year legal battle to stave off bankruptcy. At his bankruptcy hearing in 1936, he attempted to bribe judge John Warren Davis and committed perjury. In 1943, Fox served a five month and seventeen day sentence on charges of conspiring to obstruct justice and defraud the United States, in connection with his bankruptcy. After serving his time, a disgraced and embarrassed Fox retired from the film business. For many years, Fox resented the way. In 1933, he collaborated with the writer Upton Sinclair on a book Upton Sinclair Presents William Fox in which Fox recounted his life, stating his views on what he considered to be a large Wall Street conspiracy against him, his death in 1952 at the age of 73 went unnoticed in New York City. No one from Hollywood attended his funeral. Fox is interred at Brooklyn. Fox oversaw the construction of many Fox Theatres in American cities including Atlanta, Oakland, San Francisco and San Diego.
His companies had an estimated value of $300,000,000 and he owned 53 percent of Fox Film and 93 percent of the Fox Theaters. Fox had two daughters. Gabler, Neal. An Empire of Their Own: How the Jews Invented Hollywood. Crown. ISBN 0-385-26557-3. Krefft, Vanda; the Man Who Made the Movies. Harper. ISBN 9780061136061. William Fox on IMDb Historical Article on William Fox William Fox at Find a Grave
Growth arrest and DNA-damage-inducible protein GADD45 gamma is a protein that in humans is encoded by the GADD45G gene on chromosome 9. GADD45G is known as CR6, DDIT2, GRP17, OIG37, GADD45gamma. GADD45G is involved in several different processes, including sexual development, human-specific brain development, tumor suppression, the cellular stress response. GADD45G interacts with several other proteins that are involved in DNA repair, cell cycle control and senescence. Low expression of GADD45G has been associated with many types of cancer. GADD45G was cloned by Beadling under the name CR6 in 1993. In this experiment, several genes including GADD45G were noted for being induced by IL-2, they were identified as immediate early response genes in T lymphocytes, its role as a tumor suppressor was discovered in 1999 by Zhang. It received the name OIG37 from Nakayama due to its regulation by Oncostatin M, found to be able to inhibit growth, it became known as Gadd-related protein 17 during its isolation from a cDNA library by Suzuki due to its homology with Gadd45.
GADD45G is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The protein encoded by this gene responds to environmental stresses by mediating activation of the p38/JNK pathway via MTK1/MEKK4 kinase. GADD45G is in turn regulated upstream by NF-κB; the crystal structure of GADD45G reveals a dimer made of four parallel helices. The central region contains a acidic patch where it allows for interaction with cdc2, PCNA, p21; the parallel isoform of GADD45G is the active form. This gene plays a role in cell cycle regulation. GADD45G prevents the kinase ability of the cyclin b1/Cdk1 complex in a fashion that does not break apart the complex, it plays a role in the activation of the G2/M checkpoints. In the male sexual development pathway, GADD45G is essential for activating SRY, leading to proper formation of the gonads and sex-determination; this could occur through GADD45G interaction with the p38 MAPK signaling pathway.
Deletion of an enhancer close to the GADD45G gene is correlated to increased proliferation of neuronal cells, which could account for part of the difference in neural development between humans and other species. The deletion of the enhancer reduces the expression of the gene in the forebrain allowing for more brain growth in humans. GADD45G is involved with dental epithelial cell proliferation. GADD45G is expressed in enamel knots, where it regulates cell growth; the gene modulates p21-mediated epithelial cell proliferation by activating the p38 MAPK pathway during the development of teeth. There is differential expression of the Xenopus homolog of GADD45G in embryonic development, it plays a large role in neural and brain development with GADD45A. GADD45G and GADD45A knockdowns are related to improper gastrulation, defective head growth, shorter axes. GADD45G and GADD45A act redundantly to control cell growth, allow the cells to move from pluripotentcy helping cells differentiate. During a learning experience, a set of genes is expressed in the brain.
This induced gene expression is thought to be important for processing the information being learned. Such genes are known as immediate early genes. Within the prelimbic prefrontal cortex, the GADD45G gene is expressed and is required for the consolidation of a type of learning in mice termed associative fear memory. In general, gene expression can be epigenetically induced by demethylation of 5-methylcytosine in gene promoter regions; the GADD45G protein functions in repair of DNA damage. GADD45G may be involved in recognition of 5-methylcytosine as an alteration in DNA that needs to be repaired to allow induction of learning-related genes, thus GADD45G may guide the rapid demethylation of methylcytosine in the promoter regions of learning-related genes by a DNA repair process. GADD45G carries out its many stated functions with many different interactions. GADD45G was found to inhibit Cdk1 kinase activity, it interacts with CRIF, which causes the inhibition of Cdc2-cyclin B1 and Cdk-cyclin E. GADD45 works with the cyclin-dependent kinase inhibitor p21, which can cause growth arrest as well.
GADD45G is found to be involved with the p38 MAPK pathway through interactions with MAP3K4, which can be important in sex-determination. Additionally, GADD45G regulates DNA replication and repair through its interactions with PCNA. In humans, GADD45G is expressed most in the skeletal muscle and liver; this gene has a low expression in the heart, spleen and testis. GADD45G is expressed in the placenta. In the embryonic mouse, Gadd45g is expressed in the neural tube and dorsal root ganglia and the dorsal midbrain. Mammalian renal inner medullary cells face and resist hypertonic stress; such stress causes DNA damage. All three GADD45 isoforms GADD45A, GADD45B, GADD45G are induced by acute hypertonicity in murine IM cells. Maximum induction occurs 16-18 h after the onset of hypertonicity. GADD45G is induced more than GADD45B and GADD45A. Hypertonicity of various forms always induces GADD45 transcripts, whereas non-hypertonic hyperosmolality has no effect. Actinomycin D does not prevent hypertonic GADD45 induction, indicating that mRNA stabilization is the mechanism that mediates this induction.
In numerous kinds of cancerous cells, GADD45G is down regulated. There is a low expression due to methylation of the GADD45G promoter; this low expression can
China Taiping Insurance Holdings Company Limited China Insurance International Holdings Company Limited, is a Chinese insurance conglomerate. The company has strong Chinese Central Government background despite incorporated in Hong Kong, it is considered as a red chip company. The group's major businesses are reinsurance, life insurance and casualty insurance, asset management, reinsurance brokerage, pension management, real estate manager and etc; as of 2018 financial year, most of the profit of the listed company came from life insurance. More than 93% income was derived from Mainland China. According to S&P Global Ratings, citing China Insurance Regulatory Commission, market share of China Taiping's subsidiary Taiping General Insurance Co. Ltd. in property and casualty insurance in the first half of year 2017 was 2.0% and ranked the eighth. While in life insurance, the market shares of China Taiping's subsidiary Taiping Life Insurance was 3.8% and ranked ninth. While in Hong Kong, the group's China Taiping Insurance Company Limited was ranked the fourth in 2018 for its 6.0% market share by gross written premiums in general insurance market.
In reinsurance, the HK-based Taiping Reinsurance, had a market share of 17.0% in 2005. In January 2018, Taiping Trustees, a second-tier subsidiary of China Taiping Insurance Holdings, partnered with other investors, bought an office building on 18 King Wah Road in North Point; as of December 2018, the headquarter of the listed company is located on the 25/F of that building. The headquarters was located in China Taiping Tower in Causeway Bay. Taiping Financial Holdings known as China Insurance Group Securities Holdings, a Hong Kong incorporated company owned Taiping Securities, a securities broker and financial service company, it was founded in 1986 as New Century Securities, by the Bank of China Group. The company renamed to China Insurance Group Securities in 2001 and the current name in 2009. Despite the listed company was incorporated in 2000 in Hong Kong, the history of the group could be traced back to Taiping Insurance Company founded in Shanghai in 1929. Another predecessor, China Insurance Company, was founded in 1931 by the Bank of China.
Ming An Insurance Hong Kong, privatized by the listed company in 2009, first founded in Hong Kong in 1947. After the establishment of the People's Republic of China in 1949, the Bank of China, the Taiping Insurance Company and the China Insurance Company were nationalized by the Chinese Government, became part of the People's Bank of China and the People's Insurance Company of China respectively. However, the Chinese government owned bank and insurance companies still do business in Hong Kong, at that time a colony of the British Empire on Chinese soil; the Hong Kong headquarters of China Insurance Company and Ming An Insurance were located in the Bank of China Building in the 1960s, while the Hong Kong headquarters of Taiping Insurance was in Takshing House. The three aforementioned Hong Kong based Chinese government owned insurers had formed China Reinsurance Company, Limited in 1980, one of the initial major assets of the listed company, incorporated in 2000. In 1999 PICC was break down into several smaller insurer groups, including the listed company's parent company China Insurance Company, as well as PICC itself, China Life and China Re.
They were the market leaders in general insurance, life insurance and reinsurance in Mainland China respectively. Under the breakup plan, China Insurance Company was focused on overseas businesses, receiving overseas assets from PICC. China Insurance International Holdings Company Limited became a listed company in 2000. At that time Swiss Re acquired 9.9% shares of the newly listed company. According to the first annual report, most of the revenue of the listed company in year 2000, came from reinsurance. At that time Ming An Insurance HK was not yet acquired, Taiping Insurance was not yet re-established their businesses in Mainland China. Moreover, Taiping was owned by China Insurance Company, the parent company of the listed company at that time. In 2001, China Insurance Company was authorized to re-open businesses in Mainland China as an insurer. In September 2001, the listed company acquired the controlling stake of the Mainland incorporated Taiping Life from the parent company China Insurance Company, for about HK$522 million in cash and newly issued share of the listed company.
As of 2004, the listed company owned 30% of Tai Ping Insurance, a property and casualty insurer of Mainland China. As of 2018, the listed company owned 75.10% stake of the aforementioned Taiping Life as well as 100% stake of the aforementioned Taiping General Insurance. From 2002 to 2013, the listed company acquired more assets from the parent company as part a reverse IPO. In 2002, the listed company acquired China Insurance Group Assets Management Limited for about HK$403 million in cash and newly issued share of the listed company; the listed company was renamed to the current name in 2009. In the same year the company privatized fellow listed company Ming An. Ming An Insurance, owned by Ming An, was renamed to China Taiping Insurance Company Limited in November 2009. In 2013, more assets were acquired by the listed company from the parent to complete
This article provides information on candidates who stood for the 1998 Queensland state election, held on 13 June 1998. On 3 February 1996, Frank Tanti was elected to succeed Ken Davies, unseated by the Court of Disputed Returns on 8 December 1995, as the member for Mundingburra. On 5 October 1996, Paul Lucas was elected to succeed Tom Burns, who resigned on 16 May 1996, as the member for Lytton. On 24 May 1997, Linda Lavarch was elected to succeed Margaret Woodgate, who resigned on 17 March 1997, as the member for Kurwongbah. Len Ardill MLA Clem Campbell MLA Keith De Lacy MLA Wayne Goss MLA Glen Milliner MLA Geoff Smith MLA Di McCauley MLA Mark Stoneman MLA Sitting members are shown in bold text. Successful candidates are highlighted in the relevant colour. Where there is possible confusion, an asterisk is used. Members of the Queensland Legislative Assembly, 1995–1998 Members of the Queensland Legislative Assembly, 1998–2001 1998 Queensland state election Psephos: Adam Carr's Election Archive - Queensland 1998
Slide Hollow is a tributary of Panther Run in Union County, Pennsylvania, in the United States. It is 1.2 miles long and flows through Lewis Township and Hartley Township. The watershed of Slide Hollow has an area of 0.61 square miles. A total of 35 different dissolved elements have been detected in it. Wild trout naturally reproduce within the stream and it has been stocked with trout in the past. Slide Hollow begins in Middle Ridge in Lewis Township, it flows west-southwest and immediately enters Hartley Township. It continues flowing west-southwest for several tenths of a mile; the stream turns west-northwest for a short distance before turning southwest. Several tenths of a mile further downstream, it reaches its confluence with Panther Run at The Hook. Slide Hollow joins Panther Run 0.46 miles upstream of its mouth. The field pH of Slide Hollow was once measured to be 6.85, while the lab pH was measured to be 6.51. The concentration of aluminum in the stream was measured to be 12 micrograms per litre.
The concentration of dissolved oxygen was 9.39 milligrams per litre, the specific conductivity was 24 micro-siemens per centimeter. The concentrations of sulfate and chloride were 0.495, 3.548, 1.148, respectively. A total of 35 dissolved elements have been observed in the stream at concentrations above or at their detection limits. In a 2006 study, the sodium and potassium concentrations in Slide Hollow were 317 and 710 micrograms per litre, respectively; the rubidium concentration was only 0.728 micrograms per litre, however. The magnesium concentration was 1,100 micrograms per litre, the calcium concentration was 1,300 micrograms per litre; the strontium and barium concentrations were lower, only 5.68 and 11.9 micrograms per litre. In the 2006 study, the vanadium concentration in Slide Hollow was 0.1 micrograms per litre. The manganese concentration was 1.9 micrograms per litre, the cobalt concentration was 0.022 micrograms per litre, the nickel and copper concentrations were both 0.8 micrograms per litre.
The concentration of zinc was 2.7 micrograms per litre. The concentration of yttrium was 0.038 micrograms per litre and the cadmium concentration was 0.02 micrograms per litre. All of the non-radioactive lanthanides were detected in the stream, with the exception of thulium and lutetium. Concentrations ranged from 0.001 micrograms per litre to 0.024 micrograms per litre. The highest-numbered transition metal to be observed in concentrations above the detection limit was hafnium. However, the concentration of lead was 0.03 micrograms per litre and the uranium concentration was 0.006 micrograms per litre. The silicon concentration was 2,300 micrograms per litre. However, the arsenic concentration was only 0.08 micrograms per litre and the antimony concentration was 0.01 micrograms per litre. The concentration of bromine was 12 micrograms per litre, while the iodine concentration was 1 microgram per litre; the elevation near the mouth of Slide Hollow is 1,427 feet above sea level. The elevation of the stream's source is between 1,680 feet above sea level.
The watershed of Slide Hollow has an area of 0.61 square miles. The stream and its valley are within the United States Geological Survey quadrangle of Hartleton; the valley of Slide Hollow was entered into the Geographic Names Information System on August 2, 1979. Its identifier in the Geographic Names Information System is 1187806. Slide Hollow is an unofficially named stream, named after the valley through which it flows; the stream is known as Slide Hollow Run. Wild trout reproduce in Slide Hollow from its headwaters downstream to its mouth. In the 1930s, the stream was known to be a good brook trout stream, it was stocked with trout during this time. In a 2006 survey, eight fish were observed in Slide Hollow. List of rivers of Pennsylvania
There are at least two runic inscriptions in Hagia Sophia's marble parapets. They may have been engraved by members of the Varangian Guard in Constantinople in the Viking Age; the first runic inscription was discovered in 1964 on a parapet on the top floor of the southern gallery, the discovery was published by Elisabeth Svärdström in "Runorna i Hagia Sofia", Fornvännen 65, 247-49. The inscription is worn down so nowadays only -ftan, the Norse name Halfdan, is legible; the remainder of the inscription is considered to be illegible, but it is possible that it followed the common formula "NN carved these runes". A second inscription was discovered by Folke Högberg from Uppsala in 1975, it was discovered in a niche in the northern part of the same gallery as the first inscription. The discovery was reported to the Department of Runes in Stockholm in 1984, but it was not published; the archaeologist Mats G. Larsson discovered the runes anew in 1988 and published the find in "Nyfunna runor i Hagia Sofia", Fornvännen 84, 12-14.
He read ari:k and interpreted it as a possible "Ári m" or "Ári m". Because of the uncertainty in the reading, the inscription was not registered in the periodical Nytt om runer 4 of 1989. Högberg had made a different reading from Larsson in 1975, this reading was supported by Svein Indrelid, a professor of archaeology at the University of Bergen in 1997; the reading of Högberg and Indrelid is the man's name Árni and they consider the inscription to be pure graffiti, unlike Larsson. The latter learnt of Högberg's interpretation in 1989. Professor Indrelid made copies of five possible runic inscriptions on the parapet and he handed them over to the Norwegian Runic archive in 1997. There may be additional runic inscriptions waiting to be found on the walls and other parts of the Hagia Sophia. Berezan' Runestone Greece runestones Italy runestones Piraeus Lion James E. Knirk, Runer i Hagia Sofia i Istanbul, Nytt om runer 14, 26-27 Relics Of The Varangians - Grafitti in Hagia Sophia