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Arthur Kennedy

John Arthur Kennedy was an American stage and film actor known for his versatility in supporting film roles and his ability to create "an exceptional honesty and naturalness on stage" in the original casts of Arthur Miller plays on Broadway. He won the 1949 Tony Award for Best Featured Actor in a Play for Miller's Death of a Salesman, he won the Golden Globe for Best Supporting Actor for the 1955 film Trial, was a five-time Academy Award nominee. Kennedy was born on February 17, 1914, in Worcester, the son of Helen and J. T. Kennedy, a dentist, he attended South High School and Worcester Academy. At Carnegie Institute of Technology, Pittsburgh he studied drama, graduating with a B. A. in 1934. Kennedy moved to New York and, joined the Group Theatre, he toured with a classical repertory company. In September 1937, he made his Broadway debut as Bushy in Maurice Evans' Richard II at the St. James Theatre. In 1939 he played Sir Richard Vernon in Evans' Henry IV, Part 1. Kennedy made his entry into films.

His first film role was of Cagney's younger brother in City for Conquest in 1940. He was adept as hero or villain, was noted for his mastery of complex, multifaceted roles, he appeared in police dramas. During World War II, Kennedy served from 1943 to 1945 in the United States Army Air Forces making aviation training films, both as a narrator and an actor. Many of those films serve as historical records of how aviators were trained and flight equipment was operated. Kennedy appeared in many notable films from the early 1940s through mid-1960s, including High Sierra, They Died with Their Boots On, The Glass Menagerie, The Desperate Hours, Peyton Place, Some Came Running, Elmer Gantry, The Man from Laramie, Lawrence of Arabia, Nevada Smith and Fantastic Voyage. Of Kennedy's film work, he is best-remembered for his collaborations with director Anthony Mann and co-star James Stewart on Bend of the River and The Man from Laramie, in both of which he played sympathetic villains, he enjoyed a distinguished stage career over the same period, receiving a Tony Award for his role of Biff Loman in Arthur Miller's Death of a Salesman.

He inaugurated three other major characters in Miller plays: Chris Keller in All My Sons, John Proctor in The Crucible and Walter Franz in The Price. In 1961 he played the title role in Becket, opposite Laurence Olivier as Henry II. On February 5, 1959, Kennedy appeared on the episode "Make It Look Good" of CBS's Dick Powell's Zane Grey Theatre. In 1974, Kennedy was a regular on the short-lived ABC police drama Nakia, as Sheriff Sam Jericho. With the death of his wife in 1975, failing eyesight and thyroid cancer, Kennedy was reported as having lost interest in filmmaking. After Covert Action, his next films were The Humanoid and Signs of Life. In 1949, Kennedy won a Tony Award for best supporting actor as Biff in Arthur Miller's Death of a Salesman at the Morosco Theatre; the New York Film Critics named him Best Actor for Bright Victory. His performance in Trial won him a Golden Globe Award for Best Supporting Actor, his portrayal of the newspaper reporter in Elmer Gantry gained him a Film Daily Award and a Limelight Award.

Kennedy, Claude Rains and Robert Duvall share the record of four losing nominations for the Academy Award for Best Supporting Actor, although Duvall won for Best Actor in 1983. Kennedy received a nomination for Best Actor for his performance in Bright Victory. Kennedy married Mary Cheffey in March 1938, they had two children: Terence. During the last years of his life, Kennedy suffered from thyroid eye disease, he spent much of his life in Savannah, out of the public eye. He died in 1990 in Connecticut of a brain tumor, he was buried in Woodlawn Cemetery, near his home at Nova Scotia, Canada. Arthur Kennedy at the Internet Broadway Database Arthur Kennedy on IMDb Arthur Kennedy at the TCM Movie Database Arthur Kennedy at Find a Grave Photographs of Arthur Kennedy tombstone, Nova Scotia. Literature on Arthur Kennedy

WOXL-FM

WOXL-FM is a radio station licensed to Biltmore Forest, North Carolina, United States, the station serves the Asheville area and broadcasts a Hot adult contemporary music format. The station is owned by Saga Communications of North Carolina, LLC. In August 1987, the FCC allocated a new frequency, 96.5 FM, to the town of Biltmore Forest, near Asheville. Thirteen applicants filed during the filing window. One of the applicants was a small family-owned company headed up by Zeb Lee. Lee had operated 1230 AM WSKY in Asheville for many years and had felt that the FM was the future medium for radio listening; because of the number of applicants, the FCC arranged a hearing in 1989. During that time Orion tried to negotiate with the other applicants, offering up to 2 million dollars at one point, which they declined. In 1990 and 1991, the FCC's Administrative Law Judge and Review Board had both ruled in favor of Orion Broadcasting based on their track record of public affairs with WSKY and awarded the station's construction permit on the condition that WSKY was sold.

The station signed on July 29, 1994 under test authority as WZLS with a classic rock-leaning album rock format under the "Z96.5" handle. After the sound of a ticking clock, The first song was "FM" by Steely Dan. In the meantime, some of the other applicants for the license had merged to form a group called Biltmore Forest Radio Inc. headed up by U. S. House Representative Mel Watt; the group was successful in pointing out in the U. S. Court Of Appeals in a separate case Bechtel v. FCC that the FCC's "interrogation preference" was "arbitrary and capricious"; this ruling forced the FCC to place a freeze on new station licenses for a time and to revoke Orion's construction permit for WZLS. On June 2, 1997, after several appeals, WZLS was forced off the air by midnight. Biltmore Forest Radio's WZRQ signed on that same day under a time-brokered agreement with Styles Broadcasting out of Panama City, Florida. For a period of 12 hours, both stations were broadcasting at the same time, which caused interference with each other since they were on the same frequency.

WZRQ had featured a similar Album Rock format to what WZLS had, with the exception that it was voice-tracked. In the meantime, U. S. Senator Jesse Helms appealed to the U. S. Court Of Appeals on Orion Broadcasting's behalf, was successful in getting the construction permit returned to the Lee family. On January 17, 1998, WZRQ shut down by court order and WZLS returned to the airwaves after a seven-month absence, with a ticking clock and "FM" by Steely Dan. During its absence, station revenue and personnel were lost. On August 1 of that same year, Zeb Lee died, his family carried on in operating WZLS. During the time that WZLS was off the air, a rider was attached to the 1997 Balanced Budget Bill by Arizona Senator John McCain which required that new radio and TV frequency licenses were to be auctioned off to the highest bidder. Since WZLS was operating under a construction permit and had not been licensed yet, the frequency was placed on the market, it was awarded to Liberty Productions, the highest bidder.

Orion Broadcasting, forced to bid on their own station, came in third. With less than nine hours notice, on February 21, 2002, WZLS was forced off the air by the FCC. Now under the ownership of Liberty Productions, which had leased out the airtime to Saga Communications, the 96.5 frequency stunted over a period of several days with different formats. After the stunting ended, WOXL signed on with an oldies format under the name "Oldies 96.5". In its first Arbitron ratings period, the station debuted in first place; because of its limited signal due to the area's mountainous terrain, the station added a simulcast partner as 970 WWIT in nearby Canton was purchased in 2003, becoming WOXL. That station airs another station's programming. Within a few years, WOXL-FM's ratings started to drop and the station adjusted its format many times, notably to more 70s-based hits as "96.5 WOXL" rock-leaning Classic Hits as "Classic Hits 96.5", keeping the WOXL-FM callsign. On December 25, 2008, the station flipped to Adult Contemporary as "Mix 96.5."

As of 2016, its slogan changed to "Asheville's Hit Music Station", to compete more with CHR/Top 40-formatted station, WQNQ, "Star 104.3". Despite this, WOXL-FM adjusted their format to Hot AC, still plays some songs from the 1990s. Query the FCC's FM station database for WOXL Radio-Locator information on WOXL Query Nielsen Audio's FM station database for WOXLQuery the FCC's FM station database for W247BV Radio-Locator information on W247BV Query the FCC's FM station database for W251AO Radio-Locator information on W251AO

Glycogen storage disease type I

Glycogen storage disease type I is the most common of the glycogen storage diseases. This genetic disease is characterized by an impairment in liver's ability to mobilize stored glycogen to maintain adequate blood glucose. While all GSD I patients share this feature, there are two major subclassifications: GSD Ia, GSD Ib; these two conditions are bear distinctions in cause and treatment. GSD Ia is caused by a deficiency enzyme glucose-6-phosphatase, GSD Ib is caused a deficiency in glucose-6-phosphate translocase. Additionally, GSD Ib features chronic neutropenia resulting from abnormalities in the bone marrow. GSD I has an incidence of 1 in 100,000 births in the American population, 1 in 20,000 births among Ashkenazi Jews; the deficiency in GSD I impairs the ability of the liver to produce free glucose from glycogen through glycogenolysis. Since this is the principal metabolic mechanism by which the liver supplies glucose to the body during periods of fasting, the deficiency causes severe hypoglycemia.

Over time, this results in some cases the kidneys. GSD I patients present have hepatomegaly from non-alcoholic fatty liver disease as the result of excess glycogen storage. Other functions of these organs are intact in GSD I, but are susceptible to a variety of secondary problems depending on treatment. Without proper treatment, GSD I gives rise to chronic hypoglycaemia, which can result in derangements including lactic acidosis and hyperlipidemia. Frequent feedings of cornstarch or other carbohydrates are the principal treatment for all GSD I. Other therapeutic measures are needed for associated problems. GSD Ib presents with additional chronic neutropenia resulting from a dysfunction in the production of neutrophils within the bone marrow. Untreated, GSD Ib patients suffer from chronic neutropenia and neutrophil dysfunction, making them susceptible to infection. Filgrastim administered subcutaneously once daily, is the principal treatment for this feature of GSD Ib. Use of this medication results in chronic splenomegaly in GSDIb patients, increasing with dose volume.

With treatment, patients require additional treatment for frequent infections. GSD Ib patients may present with inflammatory bowel disease; the disease was named after German doctor Edgar von Gierke, who first described it in 1929. Early research into GSD type I identified numerous clinical manifestations, which were falsely thought to be primary features of the genetic disorder. However, continuing research has identified only one or two fundamental abnormalities caused by the genetic condition, which exist prior to clinical manifestations. Impairment in the liver's ability to convert stored glycogen into glucose through gluconeogenisis impairment of the neutrophil's ability to receive glucose, resulting in neutropenia and neutrophil dysfunction in GSD IbThese fundamental abnormalities give rise in a small number of primary clinical manifestations, which constitute the primary features considered in the diagnosis of GSD type I. hepatomegaly from non-alcoholic fatty liver disease cause by glycogen accumulation in the liver hypoglycaemia due to an inability to maintain adequate blood glucose levels after the time carbohydrates are absorbed increased infection risk resulting from neutropenia and neutrophil dysfunction in GSD IbPatients present with a number of secondary clinical manifestations linked to one or more of the primary clinical manifestations of GSD type I. hyperuricemia caused by low serum insulin levels resulting from prolonged hypoglycaemia, which increases the risk of gout or kidney damage hyperlactatemia caused by prolonged hypoglycaemia, in extreme cases leading to lactic acidosis hepatic adenomas developing in adulthood with unknown etiology, suspected to be caused by blood glucose dysregulation in the presence of non-alcoholic fatty liver disease inflammatory bowel disease caused neutropenia and neutrophil disfunction in GSD Ib, exacerbated by increased carbohydrate intake required to maintain adequate blood glucose levelsAdditionally, there are a number of clinical manifestations that result from the treatment of primary clinical manifestations in GSD type I. pancreatic hypertrophy caused by frequent engagement of the insulin response, resulting from increased consumption of carbohydrate to treat hypoglycaemia splenomegaly caused by sequestration of blood factors in the spleen, resulting from long-term use of Filgrastim to treat neutropenia in GSD Ib thrombocytopenia caused by the sequestration of platelets in the spleen, resulting from long-term use of Filgrastim to treat neutropenia in GSD Ib and caused or exacerbated by uncontrolled inflammatory bowel disease in either variant of GSD Type I anemia caused by sequestration of haemoglobin in the spleen, resulting from long term use of Filgrastim to treat neutropenia in GSD Ib and caused or exacerbated by uncontrolled inflammatory bowel disease in either variant of GSD Type I Hypoglycemia is the primary clinical symptom common to both GSD Ia and GSD Ib and most prompts initial diagnosis of the disease.

During fetal development in utero, maternal glucose transferred across the placenta prevents hypoglycemia. However, after birth, the inability to maintain blood glucose from stored glycogen in the liver will result in measurable hypoglycemia in no more than a 1–2 hours after feedings. Without proper dietary treatment after birth, prolonged hypoglycemia leads to lactic acidosis fulminant enough to induce primary respiratory distress in the newborn period, as well as ketoacidosis. Neurological manifestations of hypoglycemia are less severe among GSD I than in other instances. Rather than acute hypoglycemia, GSD I patients experience persisten