title: The Hardy Boys

text: ABC aired another series featuring the Hardy Boys, "The Hardy Boys/Nancy Drew Mysteries", from 1977 to 1979. The prime-time series starred Parker Stevenson and Shaun Cassidy as Frank and Joe Hardy; Pamela Sue Martin and later Janet Louise Johnson played Nancy Drew. During the first season, the series alternated between episodes featuring the Hardy Boys one week and Nancy Drew the next. The Hardy Boys were cast as young adults (Stevenson and Cassidy were 24 and 18, respectively, during the filming of the first episodes). The series featured original plots as well as ones based on "Hardy Boys" books, among them "The Clue of the Screeching Owl", "The Disappearing Floor" and "The Flickering Torch Mystery". The series received an Emmy nomination and featured a number of guest stars, including Kim Cattrall, Ray Milland, Howard Duff, and Ricky Nelson. During the second season, the series format changed to focus more on the Hardy Boys, Nancy Drew appearing mostly in crossover episodes with the brothers; midway through production of the second season, Martin quit and was replaced by Johnson. The series returned for a third season, dropping the Nancy Drew character completely and shortening its title to "The Hardy Boys".


title: The Hardy Boys

text: In 1995, another TV adaptation, simply called "The Hardy Boys", was produced by Canadian company Nelvana (normally an animation firm), syndicated by New Line Television, and dubbed in French for airing in Quebec and France as well as in the United States. Colin Gray starred as Frank Hardy and Paul Popowich played Joe. The characters were portrayed as in their early 20s, with Frank working as a reporter and Joe still in college. The show lasted for only one season of 13 episodes due to poor ratings; a series based on "Nancy Drew" that ran alongside it in syndication suffered the same fate.


title: The Hardy Boys

text: "The Hardy Boys" streaming series is a teen and young adult-oriented drama starring Rohan Campbell as Frank and Alexander Elliot as Joe released on December 4, 2020, by Hulu with Joan Lambur and Steve Cochrane executive producing the series and Jason Stone directing. Shot in Toronto, Hamilton, and other Southern Ontario locations, the 13 episodes were released on Hulu on December 4, 2020, in the United States and airs on YTV in Canada in 2021. Season 2 premiered in 2022.


title: The Hardy Boys

text: In 1970 and 1972, Gold Key Comics put out four comic-book issues tied to the 1969/71 television series.


title: The Hardy Boys

text: In March 2017, Dynamite Entertainment released Anthony Del Col’s reboot of classic characters Nancy Drew and the Hardy Boys with "Nancy Drew & The Hardy Boys: The Big Lie". Del Col has been a lifelong fan of the characters and was successful in working with Simon & Schuster to secure the comic book rights and then pitch to publishers.


title: The Hardy Boys

text: Inspired by Archie Comics’ "Afterlife with Archie", Del Col said, "So, then I started to think, 'Huh, I wonder what other characters are out there that are well-known that could be rebooted like that.' That's when I started to look around and I looked in some properties, and then I thought, 'Wait a minute. Nancy Drew. Hardy Boys. Oh, that would be really cool to do a hard-boiled noir take on them.


title: The Hardy Boys

text: The series, a hardboiled noir take on the characters, finds characters Frank and Joe Hardy accused of murdering their father, Fenton Hardy, and turning to a femme fatale-esque Nancy Drew to clear their names. The series features artwork by Italian artist Werther Dell’Ederra with covers by UK artist Fay Dalton. Del Col credits editors Matt Idelson and Matt Humphreys with helping him shape the direction of the series.


title: The Hardy Boys

text: The series debuted to positive reviews. Comics blog Readingwithaflightring.com declared it “the best 'modern' approach to updating a franchise like this that I’ve seen. It works on every level and still fully embraces the heart of who they are." Aintitcool.com reviewer Lyz Reblin stated, “The strength of the series thus far is Ms. Drew, who was absent for most of the first issue. She is a pitch-perfect modernized femme fatale, who could hold her own up against any present-day Sam Spade, Philip Marlowe, or the like.”


title: The Hardy Boys

text: The Hardy Boys have been called "a cultural touchstone all over the world." Their adventures have been continuously in print since 1927. The series was an instant success: by mid-1929 over 115,000 books had been sold, and as of 2008 the books were selling over a million copies a year (the first "Hardy Boys" book, "The Tower Treasure", alone sells over 100,000 copies a year). Worldwide, over 70 million copies of Hardy Books have been sold. A number of critics have tried to explain the reasons for the characters' longevity.


title: The Hardy Boys

text: One explanation for this continuing popularity is that the Hardy Boys are simple wish fulfillment. Their adventures allow readers to vicariously experience an escape from the mundane. At the same time, Frank and Joe live ordinary lives when not solving mysteries, allowing readers to identify with characters who seem realistic and whose parents and authority figures are unfailingly supportive and loving. The Hardy Boys also embody an ideal of masculinity: by their very name they "set the stage for a gentrified version of hardiness and constructed hardiness as an ideal for modern American males", part of the "cultural production of self-control and mastery as the revered ideal for the American man." More controversially, to Meredith Wood, the characters embody not just an ideal of masculinity, but an ideal of white masculinity. She argues that "racist stereotypes are ... fundamental to the success of the "Hardy Boys" series." In support of this claim, Wood cites what she says is the replacement of one stereotype (evil Chinese) with another (evil Latin Americans) in the original and revised versions of "Footprints Under the Window". She further claims that this is the reason for the popularity of the Applewood Books reprints of the original, unrevised texts rather than the widely cited blandness of the rewrites.


title: The Hardy Boys

text: Critic Gary Westfahl considers the Hardy Boys to not display any sexuality. The Hardys' ignorance of sex and their increasing respect for the law have led to some negative perceptions and many parodies of the characters. They are "well-scrubbed Boy Scout types" who "fetishized squareness." They have been parodied numerous times, in such works as "The Hardy Boys and the Mystery of Where Babies Come From" by Christopher Durang, "The Secret of the Old Queen: A Hardy Boys Musical" by Timothy Cope and Paul Boesing, and Mabel Maney's novel "A Ghost in the Closet: A Hardly Boys Mystery". "National Lampoon" ran an article in 1985 entitled "The Undiscovered Notebooks of Franklin W. Dixon", in which the authors "purport to have stumbled upon some unpublished "Hardy Boys" manuscripts", including "The Party Boys and the Case of the Missing Scotch" and "The Hardly Boys in the Dark Secret of the Spooky Closet."


title: The Hardy Boys

text: Others have pointed to the Hardy Boys' relationship with their father as a key to the success of the series. As Tim Morris notes, while Fenton Hardy is portrayed as a great detective, his sons are usually the ones that solve cases, making Fenton Hardy a paradoxical figure:


title: The Hardy Boys

text: He is always there, he knows everything. He is infallible but always failing. When the boys rescue him, he is typically emaciated, dehydrated, semi-conscious, delirious; they must succor him with candy bars and water. He can take on any shape but reveals his identity within moments of doing so. He never discusses a case except for the one he's working on in a given novel, so that his legendary close-mouthedness turns to garrulousness when a "Hardy Boys" novel begins, which is of course the only time we ever get to see him. All the same, he only discusses the case in enough detail to mislead his sons and put them in mortal danger. He has systems of information and data-gathering that put the FBI to shame, yet he is always losing his case notes, his ciphers, his microfilm, or some other valuable clue, usually by leaving it in his extra pair of pants, meaning that the Boys have to drive to Canada or Florida or somewhere to retrieve it. I suppose he isn't mysterious at all; he simply embodies what many think of their own fathers: utterly powerful, contemptibly inept.


title: The Hardy Boys

text: As a result, the Hardy Boys are able both to be superior to their father and to gain the satisfaction of "fearlessly making their dad proud of them."


title: The Hardy Boys

text: In the end, many commentators find that the Hardy Boys are largely successful because their adventures represent "a victory over anxiety." The "Hardy Boys" series teaches readers that "although the world can be an out-of-control place, good "can" triumph over evil, that the worst problems can be solved if we each do our share and our best to help others."


title: Jamie Redknapp

text: Jamie Frank Redknapp (born 25 June 1973) is an English former professional footballer who was active from 1989 until 2005. He is a pundit at Sky Sports and an editorial sports columnist at the "Daily Mail". A technically skillful and creative midfielder, who was also an accurate and powerful free-kick taker, Redknapp played for AFC Bournemouth, Southampton, Liverpool, and Tottenham Hotspur, captaining the latter two. He also gained 17 England caps between 1995 and 1999, and was a member of England’s squad that reached the semi finals of Euro 1996. His 11 years at Liverpool were the most prolific, playing more than 237 league games for the club, including a spell as captain, and being involved in winning the 1995 Football League Cup Final.


title: Jamie Redknapp

text: In a career that was blighted by a succession of injuries, Redknapp was as famous for his media profile off the field as much as on it. He married the pop singer Louise in 1998. Redknapp comes from a well-known footballing family. His father is the football manager Harry Redknapp. He is also a cousin of Frank Lampard, and a nephew of former West Ham United coach Frank Lampard, Sr.


title: Jamie Redknapp

text: Redknapp was born in Barton on Sea, Hampshire and started his career at Tottenham Hotspur as a youth player but turned down their offer of a contract, deciding to play for AFC Bournemouth under his father, manager Harry Redknapp. He went on to play for Liverpool where Redknapp would be remembered for his best performances. After that Redknapp returned and played two and a half seasons for Tottenham Hotspur then finally joined Southampton, where he played under his father for a second time. Redknapp was also capped 17 times by England, scoring one goal.


title: Jamie Redknapp

text: Redknapp started out on the road to professional football as a schoolboy at Tottenham Hotspur but began his professional career, at the age of 16, in 1989 at Bournemouth, then managed by his father, Harry. He made 13 appearances for the club before attracting the attention of Liverpool, who signed him on 15 January 1991. Kenny Dalglish had paid £350,000 for Redknapp, who was still only 17 at the time. He was one of the most expensively signed teenagers in English football around this time.


title: Jamie Redknapp

text: Redknapp was one of the last players to be signed by manager Kenny Dalglish before his surprising resignation on 22 February 1991 and later became the youngest Liverpool player to appear in European competition, at 18 years 120 days when making his Liverpool debut against Auxerre in the UEFA Cup on 23 October 1991, by which time Liverpool were being managed by Graeme Souness. This record was broken by Phil Charnock thirteen months later.


title: Jamie Redknapp

text: Redknapp's first goal for Liverpool came in his league debut on 7 December 1991 when he featured as a 63rd-minute substitute for Jan Mølby in a 1–1 draw with Southampton at the Dell.


title: Jamie Redknapp

text: Following Dalglish's departure, Redknapp was part of a transitional Liverpool team under Graeme Souness. He spent most of his first two-and-a-half years as a substitute or in the reserves, missing the 1992 FA Cup Final triumph and only becoming a regular first-team player in the 1993–94 season, at the expense of Mark Walters. At this time, Redknapp had also become one of the mass-marketed poster boy icons of the newly developing FA Premier League where, alongside other photogenic young players like Manchester United players Ryan Giggs and Lee Sharpe, he was used ceaselessly in commercials, advertising spots and for the league's promotional purposes in merchandising and sales, with the result being that football stars had become idols on par with rock stars and pop stars, by and around the mid to late 1990s.


title: Jamie Redknapp

text: On the pitch, Redknapp established himself as a key midfielder during the time Roy Evans managed at Anfield. He was one of a number of young players coming through the team, such as Steve McManaman and Robbie Fowler, but was criticised together with them and others like Stan Collymore and Jason McAteer as "Spice Boys" – a derogatory term that implied that the team were more interested in modelling shoots and magazine interviews than footballing success.


title: Jamie Redknapp

text: Redknapp's game revolved around being a central midfielder with a high level of ability to create space in tight situations and accurately pass his way out of them, a player who distributed the ball around the pitch with a dazzling range of passing skills, as well as having a keen eye for set pieces and long-range shooting abilities. Redknapp scored several spectacular goals in his time at Anfield and his contributions peaked during the 1998–99 season as he created numerous chances and scored 10 goals under new boss Gérard Houllier. Redknapp became vice- and then full club captain by 1999–2000 following the departures of John Barnes, Steve McManaman and Paul Ince.


title: Jamie Redknapp

text: His contributions helped the club back into the top three of the FA Premiership but a knee injury curtailed his involvement in the 2000–01 season and in a bid to cure long-standing injury troubles he underwent knee surgery under renowned knee specialist Dr Richard Steadman in the United States. As a result, Redknapp was unable to participate in the whole of the club's cup treble campaign which yielded the FA Cup, League Cup and UEFA Cup. Although injured, as the club captain he was called up by his teammates to receive the FA Cup with vice-captain Robbie Fowler at the Millennium Stadium in Cardiff. He made his comeback from injury during the pre-season tour before the 2001–02 season.


title: Jamie Redknapp

text: Redknapp's return did not last long as he was again struck by injury. On 27 October 2001 he played and scored in a 2–0 win over Charlton Athletic at The Valley, and then 3 days later he played what would prove to be his last game for the Merseyside club against Borussia Dortmund in the Champions League. He had played 308 times for the Reds and scored 41 goals, becoming a favourite amongst Liverpool fans, who included him at number 40 in the 2006 poll 100 Players Who Shook The Kop.


title: Jamie Redknapp

text: Redknapp was allowed to join Glenn Hoddle's Tottenham Hotspur on a free transfer on 18 April 2002 with just a couple of fixtures remaining of the 2001–02 season. He made his debut at the beginning of the following campaign when he played on 17 August 2002 in the 2–2 league draw with his former club Liverpool's rival Everton at Goodison Park. Redknapp's pass into the path of Matthew Etherington allowed Etherington to score his first ever Premiership goal.


title: Jamie Redknapp

text: Redknapp scored his first goal for the club a week later on 26 August 2002 in the 1–0 league win over Aston Villa at White Hart Lane. Redknapp played 49 times for Spurs scoring 4 goals in his two-and-a-half years with the club before becoming his father Harry's first signing for Southampton on 4 January 2005.


title: Jamie Redknapp

text: The 31-year-old joined Southampton's fight against relegation on a free transfer and made his debut on 5 January 2005 in the 3–3 league draw with Fulham at St Mary's. Redknapp's only goal for the club came three days later in the 3–1 FA Cup 3rd round victory over Northampton Town at Sixfields Stadium.


title: Jamie Redknapp

text: Redknapp was rarely fully fit during his brief spell at the Saints and was not able to prevent them from being relegated to the Championship after 27 successive seasons of top flight football.


title: Jamie Redknapp

text: At the end of the season, on 19 June 2005, the 31-year-old Redknapp decided to retire from the game due to his constant injury problems and on the advice of his medical specialists.


title: Jamie Redknapp

text: England manager Terry Venables gave Redknapp his international debut on 6 September 1995 in the 0–0 international friendly with Colombia at Wembley. The game is probably best remembered for his mishit cross that produced René Higuita's famous 'scorpion kick'. It ranked 94th in Channel 4's "100 Greatest Sporting Moments" in 2002.


title: Jamie Redknapp

text: Redknapp was capped 17 times for England but played just 39 minutes at a major tournament, which was during the Euro 96 campaign when he appeared as a substitute against Scotland in the group stage. Rob Smyth later wrote in "The Guardian" that Redknapp's "slick passing greased some slow-moving wheels". Injury later ruled him out of contention for both the 1998 FIFA World Cup and 2000 UEFA European Championship.


title: Jamie Redknapp

text: His only international goal came on 10 October 1999 in the 2–1 friendly victory against Belgium at the Stadium of Light, Sunderland.


title: Jamie Redknapp

text: On 21 September 2007, Chelsea reportedly approached Redknapp to become Avram Grant's assistant, as Chelsea's owner billionaire Roman Abramovich looked to shake up Stamford Bridge's coaching staff, though no appointment was forthcoming.


title: Jamie Redknapp

text: On 11 December 2008, it was announced Jamie Redknapp would become coach of Chelsea reserves two days a week whilst studying for his UEFA coaching badges. The vacancy arose after former Chelsea reserves coach Brendan Rodgers was hired by Championship outfit Watford.


title: Jamie Redknapp

text: Redknapp began his career in 2004 as a studio-based pundit on BBC during the European Championships. Since retiring he had gone into punditry full-time and is a regular studio pundit on Sky Sports alongside former England teammate Gary Neville. He is also a regular columnist on the Sky Sports website.


title: Jamie Redknapp

text: In 2005, Redknapp launched a bi-monthly magazine with his wife Louise and former teammate Tim Sherwood named "Icon Magazine", aimed at professional footballers and their families.


title: Jamie Redknapp

text: In 2010, he was made host and mentor on the Sky1 show "Football's Next Star", and a team captain in the Sky1 sports game show "A League of Their Own".


title: Jamie Redknapp

text: Redknapp has received significant attention for his repeated overuse and misuse of the word "literally", in quotes such as "he literally chopped him in half in that challenge", "Alonso and Sissoko have been picked to literally sit in front of the back four", "Drogba literally destroyed Senderos today", "in his youth, Michael Owen was literally a greyhound", "he had to cut back inside onto his left, because he literally hasn't got a right foot", "Martin Jol's head is literally on the chopping block" and "these balls now – they literally explode off your feet". In 2010, he was presented with the Foot in Mouth Award from the Plain English Campaign for his poor use of English.


title: Jamie Redknapp

text: On 22 April 2021, chat show "Redknapp's Big Night Out" premieried on Sky One, presented by Jamie and Harry Redknapp with comedian Tom Davis.


title: Jamie Redknapp

text: Redknapp's father is football manager Harry Redknapp, and his mother is Sandra Harris. He has one older brother, Mark, who is a model. He is the maternal cousin of Frank Lampard, whose father is former West Ham United player and Harry's former managerial assistant Frank Lampard, Sr.


title: Jamie Redknapp

text: Redknapp grew up on the south coast as his father was coaching Bournemouth at that time. He attended Twynham School in Christchurch and started playing in the Sunday league youth teams with his brother.


title: Jamie Redknapp

text: On 29 June 1998, Redknapp married the pop singer Louise Nurding, a member of the girl group Eternal. On 27 July 2004, Louise gave birth to a boy named Charles William "Charley" Redknapp at London's Portland Hospital. Charley was named after Louise's grandfather, who died on the day that she found out she was pregnant. On 10 November 2008, Louise gave birth to their second son, Beau Henry Redknapp. Louise revealed the name was a tribute to Jamie's father, Harry, who was born in Bow, London. The family lived in Oxshott, Surrey. After 19 years of marriage, Jamie and Louise Redknapp were granted a divorce on 29 December 2017.


title: Jamie Redknapp

text: On 18 October 2021, Redknapp married model Frida Andersson, at Chelsea Registry Office in London. The couple welcomed their first child on 24 November 2021, a boy named Raphael.


title: Oppositional defiant disorder

text: Oppositional defiant disorder (ODD) is listed in the DSM-5 under "Disruptive, impulse-control, and conduct disorders" and defined as "a pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness". This behavior is usually targeted toward peers, parents, teachers, and other authority figures. Unlike conduct disorder (CD), those with ODD do not show patterns of aggression towards people or animals, destruction of property, theft, or deceit. It has certain links to attention deficit hyperactivity disorder (ADHD), and as many as one half of children with ODD also fulfill the diagnostic criteria for ADHD.


title: Oppositional defiant disorder

text: Oppositional defiant disorder was first defined in the "DSM-III" (1980). Since the introduction of ODD as an independent disorder, the field trials to inform its definition have included predominantly male subjects. Some clinicians have debated whether the diagnostic criteria would be clinically relevant for use with women, and furthermore, some have questioned whether gender-specific criteria and thresholds should be included. Additionally, some clinicians have questioned the preclusion of ODD when conduct disorder is present. According to Dickstein, the "DSM-5" attempts to:


title: Oppositional defiant disorder

text: ODD is a pattern of negative, defiant, disobedient, and hostile behavior, and it is one of the most prevalent disorders from preschool age to adulthood. This can include frequent temper tantrums, excessive arguing with adults, refusing to follow rules, purposefully upsetting others, getting easily irked, having an angry attitude, and vindictive acts. Children with ODD usually begin showing symptoms around 6 to 8, although the disorder can emerge in younger children too. Symptoms can last throughout teenage years. The pooled prevalence is 3.6% up to age 18. While adults can be affected by ODD, they often go undiagnosed if they were not diagnosed as children. There has been research to support that ODD is more common in boys than girls with a 2:1 ratio.


title: Oppositional defiant disorder

text: Oppositional defiant disorder has a prevalence of 1% to 11%. The average prevalence is approximately 3.3%. Gender and age play an important role in the rate of the disorder. ODD gradually develops and becomes apparent in preschool years, often before the age of eight years old. However, it is very unlikely to emerge following early adolescence. There is a difference in prevalence between boys and girls, with a ratio of 1.4 to 1 before adolescence. However, girls' prevalence tends to increase after puberty. Researchers have found that the general prevalence of ODD throughout cultures remains constant. However, the difference in ODD prevalence between sexes is only significant in Western cultures. It is possible that there is a decreased prevalence of ODD in boys or an increased prevalence of ODD in girls in non-Western cultures, but it is also possible that the disorder is either over- or under-diagnosed in boys or girls, respectively, in Western cultures.


title: Oppositional defiant disorder

text: Other factors can influence the prevalence of the disorder: Youths living in families of low socioeconomic status have a higher prevalence. Another factor is based on the criteria used to diagnose an individual. When the disorder was first included in the "DSM-III", the prevalence was 25% higher than when the "DSM-IV" revised the criteria of diagnosis. The "DSM-V" made more changes to the criteria, grouping certain characteristics together in order to demonstrate that ODD display both emotional and behavioral symptoms. In addition, criteria were added to help guide clinicians in diagnosis because of the difficulty found in identifying whether the behaviors or other symptoms are directly related to the disorder or simply a phase in a child's life. Consequently, future studies may obtain results indicating a decline in prevalence between the "DSM-IV" and the "DSM-V".


title: Oppositional defiant disorder

text: The fourth revision of the "Diagnostic and Statistical Manual" ("DSM-IV-TR") (now replaced by "DSM-5") states that a person must exhibit four out of the eight signs and symptoms to meet the diagnostic threshold for ODD. These symptoms include:


title: Oppositional defiant disorder

text: These behaviors are mostly directed towards an authority figure such as a teacher or a parent. Although these behaviors can be typical among siblings, they must be observed with individuals other than siblings for an ODD diagnosis. Children with ODD can be verbally aggressive. However, they do not display physical aggressiveness, a behavior observed in conduct disorder. Furthermore, they must be perpetuated for longer than six months and must be considered beyond a normal child's age, gender and culture to fit the diagnosis. For children under five years of age, they must occur on most days over a period of six months. For children over five years of age, they must occur at least once a week for at least six months. If symptoms are confined to only one setting, most commonly home, it is considered mild in severity. If it is observed in two settings, it is characterized as moderate, and if the symptoms are observed in three or more settings, it is considered severe.


title: Oppositional defiant disorder

text: There is no specific element that has yet been identified as directly causing ODD. Research looking precisely at the etiological factors linked with ODD is limited. The literature often examines common risk factors linked with all disruptive behaviors, rather than ODD specifically. Symptoms of ODD are also often believed to be the same as CD, even though the disorders have their own respective set of symptoms. When looking at disruptive behaviors such as ODD, research has shown that the causes of behaviors are multi-factorial. However, disruptive behaviors have been identified as being mostly due either to biological or environmental factors.


title: Oppositional defiant disorder

text: Research indicates that parents pass on a tendency for externalizing disorders to their children that may be displayed in multiple ways, such as inattention, hyperactivity, or oppositional and conduct problems. Research has also shown that there is a genetic overlap between ODD and other externalizing disorders. Heritability can vary by age, age of onset, and other factors. Adoption and twin studies indicate that 50% or more of the variance causing antisocial behavior is attributable to heredity for both males and females. ODD also tends to occur in families with a history of ADHD, substance use disorders, or mood disorders, suggesting that a vulnerability to develop ODD may be inherited. A difficult temperament, impulsivity, and a tendency to seek rewards can also increase the risk of developing ODD. New studies into gene variants have also identified possible gene-environment (G x E) interactions, specifically in the development of conduct problems. A variant of the gene that encodes the neurotransmitter metabolizing enzyme monoamine oxidase-A (MAOA), which relates to neural systems involved in aggression, plays a key role in regulating behavior following threatening events. Brain imaging studies show patterns of arousal in areas of the brain that are associated with aggression in response to emotion-provoking stimuli.


title: Oppositional defiant disorder

text: Many pregnancy and birth problems are related to the development of conduct problems. Malnutrition, specifically protein deficiency, lead poisoning or exposure to lead, and mother's use of alcohol or other substances during pregnancy may increase the risk of developing ODD. In numerous research, substance use prior to birth has also been associated with developing disruptive behaviors such as ODD. Although pregnancy and birth factors are correlated with ODD, strong evidence of direct biological causation is lacking.


title: Oppositional defiant disorder

text: Deficits and injuries to certain areas of the brain can lead to serious behavioral problems in children. Brain imaging studies have suggested that children with ODD may have hypofunction in the part of the brain responsible for reasoning, judgment, and impulse control. Children with ODD are thought to have an overactive behavioral activation system (BAS), and an underactive behavioral inhibition system (BIS). The BAS stimulates behavior in response to signals of reward or non-punishment. The BIS produces anxiety and inhibits ongoing behavior in the presence of novel events, innate fear stimuli, and signals of non-reward or punishment. Neuroimaging studies have also identified structural and functional brain abnormalities in several brain regions in youths with conduct disorders. These brain regions are the amygdala, prefrontal cortex, anterior cingulate, and insula, as well as interconnected regions.


title: Oppositional defiant disorder

text: As many as 40 percent of boys and 25 percent of girls with persistent conduct problems display significant social-cognitive impairments. Some of these deficits include immature forms of thinking (such as egocentrism), failure to use verbal mediators to regulate his or her behavior, and cognitive distortions, such as interpreting a neutral event as an intentional hostile act.


title: Oppositional defiant disorder

text: Children with ODD have difficulty controlling their emotions or behaviors. In fact, students with ODD have limited social knowledge that is based only on individual experiences, which shapes how they process information and solve problems cognitively.


title: Oppositional defiant disorder

text: This information can be linked with the social information processing model (SIP) that describes how children process information to respond appropriately or inappropriately in social settings. This model explains that children will go through five stages before displaying behaviors: encoding, mental representations, response accessing, evaluation, and enactment.


title: Oppositional defiant disorder

text: This will therefore directly impact their interactions and relationship negatively. It has been shown that social and cognitive impairments result in negative peer relationships, loss of friendship, and an interruption in socially engaging in activities.


title: Oppositional defiant disorder

text: Children learn through observational learning and social learning. Therefore, observations of models have a direct impact and greatly influence children's behaviors and decision-making processes. Children often learn through modeling behavior. Modeling can act as a powerful tool to modify children's cognition and behaviors.


title: Oppositional defiant disorder

text: Negative parenting practices and parent–child conflict may lead to antisocial behavior, but they may also be a reaction to the oppositional and aggressive behaviors of children. Factors such as a family history of mental illnesses and/or substance use disorders as well as a dysfunctional family and inconsistent discipline by a parent or guardian can lead to the development of behavior disorders. Parenting practices not providing adequate or appropriate adjustment to situations as well as a high ratio of conflicting events within a family are causal factors of risk for developing ODD.


title: Oppositional defiant disorder

text: Insecure parent–child attachments can also contribute to ODD. Often little internalization of parent and societal standards exists in children with conduct problems. These weak bonds with their parents may lead children to associate with delinquency and substance use. Family instability and stress can also contribute to the development of ODD. Although the association between family factors and conduct problems is well established, the nature of this association and the possible causal role of family factors continues to be debated.


title: Oppositional defiant disorder

text: School is also a significant environmental context besides family that strongly influences a child's maladaptive behaviors. Studies indicate that child and adolescent externalizing disorders like ODD are strongly linked to peer network and teacher response. Children with ODD present hostile and defiant behavior toward authority including teachers which makes teachers less tolerant toward deviant children. The way in which a teacher handles disruptive behavior has a significant influence on the behavior of children with ODD. Negative relationships from the socializing influences and support network of teachers and peers increases the risk of deviant behavior. This is because the child consequently gets affiliated with deviant peers that reinforce antisocial behavior and delinquency. Due to the significant influence of teachers in managing disruptive behaviors, teacher training is a recommended intervention to change the disruptive behavior of ODD children.


title: Oppositional defiant disorder

text: In a number of studies, low socioeconomic status has also been associated with disruptive behaviors such as ODD.


title: Oppositional defiant disorder

text: Other social factors such as neglect, abuse, parents that are not involved, and lack of supervision can also contribute to ODD.


title: Oppositional defiant disorder

text: Externalizing problems are reported to be more frequent among minority-status youth, a finding that is likely related to economic hardship, limited employment opportunities, and living in high-risk urban neighborhoods. Studies have also found that the state of being exposed to violence was a contribution factor for externalizing behaviors to occur.


title: Oppositional defiant disorder

text: For a child or adolescent to qualify for a diagnosis of ODD, behaviors must cause considerable distress for the family or interfere significantly with academic or social functioning. Interference might take the form of preventing the child or adolescent from learning at school or making friends or placing him or her in harmful situations. These behaviors must also persist for at least six months. Effects of ODD can be greatly amplified by other disorders in comorbidity such as ADHD. Other common comorbid disorders include depression and substance use disorders. Adults who were diagnosed with ODD as children tend to have a higher chance of being diagnosed with other mental illness in their lifetime, as well as being at higher risk of developing social and emotional problems.


title: Oppositional defiant disorder

text: Approaches to the treatment of ODD include parent management training, individual psychotherapy, family therapy, cognitive behavioral therapy, and social skills training. According to the American Academy of Child and Adolescent Psychiatry, treatments for ODD are tailored specifically to the individual child, and different treatment techniques are applied for pre-schoolers and adolescents.


title: Oppositional defiant disorder

text: Children with oppositional defiant disorder tend to exhibit problematic behavior that can be very difficult to control. An occupational therapist can recommend family based education referred to as Parent Management Training (PMT) in order to encourage positive parents and child relationships and reduce the child's tantrums and other disruptive behaviors. Since ODD is a neurological disorder that has biological correlates, an occupational therapist can also provide problem solving training to encourage positive coping skills when difficult situations arise, as well as offer cognitive behavioral therapy.


title: Oppositional defiant disorder

text: Psychopharmacological treatment is the use of prescribed medication in managing oppositional defiant disorder. Prescribed medications to control ODD include mood stabilizers, anti-psychotics, and stimulants. In two controlled randomized trials, it was found that between administered lithium and the placebo group, administering lithium decreased aggression in children with conduct disorder in a safe manner. However, a third study found the treatment of lithium over a period of two weeks invalid. Other drugs seen in studies include haloperidol, thioridazine, and methylphenidate which also is effective in treating ADHD, as it is a common comorbidity.


title: Oppositional defiant disorder

text: The effectiveness of drug and medication treatment is not well established. Effects that can result from taking these medications include hypotension, extrapyramidal symptoms, tardive dyskinesia, obesity, and increase in weight. Psychopharmacological treatment is found to be most effective when paired with another treatment plan, such as individual intervention or multimodal intervention.


title: Oppositional defiant disorder

text: In one case, a 16-year-old boy was given estrogen at an L. A. juvenile jail due to allegedly having ODD due to somewhat elevated testosterone levels, developing gynecomastia and requiring breast reduction surgery as a result.


title: Oppositional defiant disorder

text: Individual interventions are focused on child-specific individualized plans. These interventions include anger control/stress inoculation, assertiveness training, a child-focused problem-solving skills training program, and self-monitoring skills.


title: Oppositional defiant disorder

text: Anger control and stress inoculation help prepare the child for possible upsetting situations or events that may cause anger and stress. They include a process of steps the child may go through.


title: Oppositional defiant disorder

text: Assertiveness training educates individuals in keeping a balance between passivity and aggression. It aims to help the child respond in a controlled and fair manner.


title: Oppositional defiant disorder

text: A child-focused problem-solving skills training program aims to teach the child new skills and cognitive processes that teach how to deal with negative thoughts, feelings, and actions.


title: Oppositional defiant disorder

text: According to randomized trials, evidence shows that parent management training is most effective. It has strong influences over a long period of time and in various environments.


title: Oppositional defiant disorder

text: Parent-child interaction training is intended to coach the parents while involving the child. This training has two phases; the first phase is child-directed interaction, where the focus is to teach the child non-directive play skills. The second phase is parent-directed interaction, where the parents are coached on aspects including clear instruction, praise for compliance, and time-out for noncompliance. The parent-child interaction training is best suited for elementary-aged children.


title: Oppositional defiant disorder

text: Parent and family treatment has a low financial cost, which can yield an increase in beneficial results.


title: Oppositional defiant disorder

text: Multimodal intervention is an effective treatment that looks at different levels including family, peers, school, and neighborhood. It is an intervention that concentrates on multiple risk factors. The focus is on parent training, classroom social skills, and playground behavior programs. The intervention is intensive and addresses barriers to individuals' improvement such as parental substance use or parental marital conflict.


title: Oppositional defiant disorder

text: An impediment to treatment includes the nature of the disorder itself, whereby treatment is often not complied with and is not continued or stuck with for adequate periods of time.


title: Oppositional defiant disorder

text: Oppositional defiant disorder can be described as a term or disorder with a variety of pathways in regard to comorbidity. High importance must be given to the representation of ODD as a distinct psychiatric disorder independent of conduct disorder.


title: Oppositional defiant disorder

text: In the context of oppositional defiant disorder and comorbidity with other disorders, researchers often conclude that ODD co-occurs with an attention deficit hyperactivity disorder (ADHD), anxiety disorders, emotional disorders as well as mood disorders. Those mood disorders can be linked to major depression or bipolar disorder. Indirect consequences of ODD can also be related or associated with a later mental disorder. For instance, conduct disorder is often studied in connection with ODD. Strong comorbidity can be observed within those two disorders, but an even higher connection with ADHD in relation to ODD can be seen. For instance, children or adolescents who have ODD with coexisting ADHD will usually be more aggressive and have more of the negative behavioral symptoms of ODD, which can inhibit them from having a successful academic life. This will be reflected in their academic path as students.


title: Oppositional defiant disorder

text: Other conditions that can be predicted in children or people with ODD are learning disorders in which the person has significant impairments with academics and language disorders, in which problems can be observed related to language production and/or comprehension.


title: Methylprednisolone

text: Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol) is a synthetic glucocorticoid, primarily prescribed for its anti-inflammatory and immunosuppressive effects. It is either used at low doses for chronic illnesses or used concomitantly at high doses during acute flares. Methylprednisolone and its derivatives can be administered orally or parenterally.


title: Methylprednisolone

text: Regardless of route of administration, methylprednisolone integrates systemically as exhibited by its effectiveness to quickly reduce inflammation during acute flares. It is associated with many adverse reactions that require tapering off the drug as soon as the disease is under control. Serious side effects include iatrogenic Cushing's Syndrome, hypertension, osteoporosis, diabetes, infection, and skin atrophy.


title: Methylprednisolone

text: Chemically, methylprednisolone is a synthetic pregnane steroid hormone derived from hydrocortisone and prednisolone. It belongs to a class of synthetic glucocorticoids and more generally, corticosteroids. It acts as a mineralocorticoid and glucocorticoid receptor agonist. In comparison to other exogenous glucocorticoids, methylprednisolone has a higher affinity to glucocorticoid receptors than to mineralocorticoid receptors.


title: Methylprednisolone

text: Glucocorticoid's name was derived after the discovery of their involvement in regulating carbohydrate metabolism. The cellular functions of glucocorticoids, such as methylprednisolone, are now understood to regulate homeostasis, metabolism, development, cognition, and inflammation. They play a critical role in adapting and responding to environmental, physical and emotional stress.


title: Methylprednisolone

text: Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and FDA approved in the United States in October 1957. In 2020, it was the 161st most commonly prescribed medication in the United States, with more than 3million prescriptions. Methylprednisolone is also on the World Health Organization's List of Essential Medicines for its effects against lymphoid leukemia.


title: Methylprednisolone

text: Methylprednisolone is a synthetic glucocorticoid (GCs) that exhibits pleiotropic effects on a variety of physiological mechanisms. However, they have been prescribed extensively for their effects on inflammation and immunity. The effects of synthetic glucocorticoids, such as methylprednisolone, is dependent on its association with intracellular glucocorticoid receptors (GRs), and to a lesser extent, mineralocorticoid receptors (MRs). GRs are widely distributed in contrast to MRs that show a restricted tissue distribution. By this mechanism, the ligand-bound receptor translocate to the nucleus and modulate gene expression.


title: Methylprednisolone

text: In the absence of endogenous or synthetic GCs, monomeric GRs are located in the cytoplasm and form multiprotein complexes with heat shock proteins (HSPs), immunophilins, and other chaperones such as src, and p23. The GR acts in a ligand-dependent manner, with the complex holding the GR in an inactive form with high specificity for the ligand. When methylprednisolone from the plasma or interstitial fluid diffuses passively across the cell membrane, it binds to the GR inducing a conformational change and GC-GR dimerization. It was previously thought that this conformational change was necessary to dissociate the multiprotein complex to allow the ligand bound receptor to translocate to the nucleus. However, recent studies have indicated that chaperones play a role in nuclear import. The now active methylprednisolone-GR complex can either transduce non-genomic changes in the cytoplasm or translocate to the nucleus and regulate transcriptional activity of target genes by direct, tethering or composite mechanisms.


title: Methylprednisolone

text: Genomic mechanisms, regardless of which type, elicit responses with a slow onset and a slow dissipation. This is attributed to the duration of mRNA transcription and translation. Glucocorticoids have the ability to regulate roughly 100 to 1000 genes with specificity to cell-type.


title: Methylprednisolone

text: Three major mechanisms have described how the MP-GR complex alter gene expression by either binding to DNA or transcription modulators. One mechanism of genomic signaling occurs when the MP-GR complex directly binds to DNA sequences called glucocorticoid response elements (GREs). GREs are located in regulatory regions of target genes and mediate their transactivation or transrepression. For example, the activation of lipocortin 1 (ANAX1) negatively interferes with the production of prostaglandins and leukotrienes, known pro-inflammatory signals. Likewise, negative GREs (nGREs) are responsible for repressing genes involved in immune cell activation.


title: Methylprednisolone

text: Post translational modifications (PTMs) also contribute to methylprednisolone signaling and can produce genomic and non-genomic effects. The GR has contains several sites for phosphorylation, sumoylation, ubiquitination, and acetylation that primarily occurs after intracellular methylprednisolone binding to the GR. PTMs modulate many functions including nuclear translocation, strength and duration of receptor signaling and cofactor interaction. A specific example is the deacetylation by histone deacetylase 2 (HDACe) was necessary for transrepression of NF-κB.


title: Methylprednisolone

text: The mechanisms of non-genomic signaling are distinct from genomic signaling, yet mediate similar pathways and provide therapeutic relevance. These mechanisms are characterized as having a rapid onset (less than 15 minutes), because they do not rely on time-consuming transcription or translation and are not modified by inhibitors of transcription.


title: Methylprednisolone

text: Methylprednisolone induced non-genomic signaling is classified by three mechanisms: (1) cytoplasmic glucocorticoid receptor (cGR)-mediated non-genomic effects, (2) membrane-bound glucocorticoid receptor (mGR) non-genomic effects, and (3) physiochemical interactions with cellular membranes (non-specific non-genomic effects).


title: Methylprednisolone

text: Proteins that dissociate from the activated GC-cGR complex, initiate intracellular transcription-independent mechanisms. It is evidence that dissociated SRC is responsible for inhibiting the release of arachidonic acid (AA) from cell membrane phospholipids. AA is required for the synthesis of inflammatory mediators (prostaglandins and leukotrienes) and thus AA inhibition mediates several important pathways such as cellular growth, metabolism and inflammation.


title: Methylprednisolone

text: Previous studies identified mGRs in lymphoma cells, but it wasn't until 2004 that mGRs were identified in human peripheral mononuclear cells. The prevalence of mGRs ranges per cell type, with the highest concentration in B lymphocytes at up to 12.3%, up to 9.2% in monocytes, and absent from T lymphocytes. Studies have shown a positive correlation between the mGR-positive cells and disease related activity. There are no proven signaling pathways associated with mGR at this time. Some researchers hypothesize that high disease activity activates mGR expression and upon administering methylprednisolone, creates a negative feedback loop by inducing apoptosis.


title: Methylprednisolone

text: High concentrations of methylprednisolone intercalate in plasma and mitochondrial cellular membranes. This association changes physiochemical properties of the membrane; activating membrane proteins, altering cellular functions and ultimately influencing cation transport through the plasma membrane and stimulating the proton leak across the inner mitochondrial membrane. Hindered oxidative phosphorylation compromises ATP production, a major energy source for cellular energy metabolism and immune function. In vivo studies of Con-A stimulated thymocytes (in rats) and human immune cells that were administered high doses of methylprednisolone has been shown to inhibit respiration in a dose-dependent manner, inhibit plasma calcium and sodium uptake, and increase cytoplasmic calcium concentration. The summative process is as follows: Methylprednisolone intercalates in the plasma membrane, causes physiochemical changes, activates membrane proteins that inhibit plasma calcium and sodium uptake (mimicking an energy deficit state). ATP consumption drops (resembled by inhibited respiration), resulting in protein permeability at the inner mitochondrial membrane and uncoupling of oxidative phosphorylation. Of notable importance, DNA/RNA synthesis was not hindered. The dependency of house keeping cells and immune cells on ATP, results in immunosuppression during ATP deficit. Specific immune functions effected by this process are cytokinesis, migration, phagocytosis, antigen processing and presenting, antibody synthesis, cytotoxicity and regulation.


title: Methylprednisolone

text: The activation of the hypothalamic-pituitary axis (HPA axis) stimulates the production of endogenous glucocorticoids within the adrenal cortex. The HPA axis interprets stimuli (stress, inflammation and circadian cues) and transduces a corresponding physiochemical response. Glucocorticoids released in the blood, serve as a messenger by binding to glucocorticoid receptors in a wide distribution across the body, including the HPA axis itself. Thus, the physiological range of GCs is monitored by the negative feedback loop GCs exert on any portion of the HPA axis. Methylprednisolone structurally and functionally mimics endogenous corticoids and will act upon the HPA axis in a similar fashion.


title: Methylprednisolone

text: Methylprednisolone is approved for oral and parenteral administration. Methylprednisolone (Medrol) for oral administration is available in a tablet formulation in 2 mg, 4 mg, 8 mg, 16 mg or 32 mg strengths. Both methylprednisolone acetate (Depo-Medrol) and methylprednisolone succinate (Solu-Medrol) are approved for intramuscular injection. Depo-Medrol is additionally approved for intralesional, intra-articular, and soft tissue injections. Depo-Medrol is available as sterile aqueous solution in 20 mg/mL, 40 mg/mL, or 80 mg/mL strengths. Solu-Medrol is the only derivative of methylprednisolone that is approved for intravenous infusion, as the sterile powder is soluble in water and can be mixed with a diluent. Strengths vary from 40 mg to 2g.


title: Methylprednisolone

text: Synthetic glucocorticoids are similar to endogenous steroids in metabolism, but differ in affinity for glucocorticoid and mineralocorticoid receptors, affinity for protein-binding, rate of elimination, and metabolic products.


title: Methylprednisolone

text: Oral methylprednisolone is readily absorbed from the gastrointestinal tract with a bioavailability of 89.9%. In contrast to endogenous GCs, methylprednisolone does not bind to the glycoprotein transcortin (corticosteroid binding globulin, CBG) but does have moderate protein binding to albumin. Thus, pharmacokinetics of methylprednisolone is linear and show no dose dependency. Patients exhibiting low albumin concentrations are at risk for adverse effects during glucocorticoid therapy. Oral methylprednisolone has a moderate distribution into tissue at 1.38L/kg.


title: Methylprednisolone

text: Methylprednisolone is primarily eliminated by hepatic metabolism and renal excretion of metabolites; with renal excretion of unchanged methylprednisolone at only 1.3–9.2%. Methylprednisolone can be interconverted with methylprednisone. Hepatic metabolism is mediated by 11 beta-hydroxysteroid dehydrogenases (11[beta]-HSD) and 20-ketosteroid reductases. Methylprednisolone undergoes renal excretion of hydrophilic inactive metabolites, including 20-carboxymelthylprednisolone and 6[beta]-hydroxy-20[alpha]-hydroxymethylprednisolone.


title: Methylprednisolone

text: As stated previously, the primary use of methylprednisolone is to suppress inflammatory and immune responses. Methylprednisolone achieves this primarily by regulating the number and function of leukocytes, cytokines and chemokines. Its widespread inflammatory control is conducive in use across multiple disorders regardless of pathology. Methylprednisolone is commonly prescribed as short-term therapy for acute flares, as seen with acute gouty arthritis. It can be prescribed during on-going therapy in lower doses contingent upon monitorization of adverse effects. Dosage strength and formulation are optimized per medical use.


title: Methylprednisolone

text: In 2001–2002, 11.4% of patients diagnosed with asthma and seen at an outpatient visit were prescribed oral corticosteroids as a long-term control therapy. The National Asthma Education and Prevention Program (NAEPP) indicates systemic methylprednisolone in both short and long term therapies to quickly control and to suppress persistent asthma, respectively. For exacerbations that result in a visit to the Emergency Department (ED), oral methylprednisolone is preferred over intravenous administration, unless there are issues with adherence or vomiting. Oral methylprednisolone is less invasive and studies have shown that equivalent efficacy compared to intravenous methylprednisolone. Dosage above 60–80 mg/day or 2 mg/kg/day is not recommended as it has not been shown to alter pulmonary function, rate of admission, or length of stay in the hospital compared to lower doses. Following ED discharge, it is advised to prescribed a five-day course of methylprednisolone to decrease the probability of relapse or withdrawal symptoms.


title: Methylprednisolone

text: Methylprednisolone is used to treat several rheumatic diseases, such as Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Methylprednisolone dosage and administration for these diseases is highly variable due to varied pathophysiology between the diseases and within patients diagnosed with a given disease. In Lupus Nephritis, a common manifestation of SLE, patients are often prescribed methylprednisolone concomitantly with immunosuppressants. Severe manifestations are often treated with Cyclophosphamide or Rituximab and three doses of methylprednisolone IV-pulse treatment (as recommended by ACR guidelines) prior to switching to oral prednisolone and azathioprine for maintenance.


title: Methylprednisolone

text: Intra-articular corticosteroid injections (IACI) are a second line therapy to relieve joint pain resulting from rheumatoid arthritis. It is most commonly injected into the joints of the knees and shoulders. Although the injection is local, studies have shown systemic absorption as evidenced by beneficial effects on distant joints. In an attempt to minimize HPA suppression, FDA guidelines have restricted IACIs to three per year, with a minimum of 30 days in between injections.


title: Methylprednisolone

text: Methylprednisolone is not typically recommended for primary or secondary adrenocortical insufficiency compared to other corticosteroids which have a higher affinity for mineralocorticoid receptor and salt retaining properties.


title: Methylprednisolone

text: Some of the off-label indications of methylprednisolone include acute spinal cord injury, acute respiratory distress syndrome, alcoholic hepatitis, hormonal resuscitation in cadaveric organ recovery, and chronic obstructive pulmonary disease.


title: Methylprednisolone

text: Signifies varying strengths of available forms. Is not indicative of frequency nor daily cumulative dose; varies per patient and condition.


title: Methylprednisolone

text: Methylprednisolone should not be taken orally by people who have systemic fungal infections, with the exception of Depo-Medrol when administered as an intra-articular injection for localized joint conditions. Methylprednisolone is contraindicated in those with known hypersensitivity to methylprednisolone or its components Steroids should be used with caution in patients with ulcerative colitis, heart disease or hypertension, peptic ulcer, renal insufficiency, osteoporosis, myasthenia gravis, glaucoma, and diabetes. Psychic manifestations may appear while taking methylprednisolone, ranging from euphoria, insomnia, personality changes to depression. Caution is required for patients with predisposed psychoses, as psychotic tendencies may be exacerbated while taking corticosteroids.


title: Methylprednisolone

text: Solu-Medrol 40 mg dosage contains lactose monohydrate produced from cow's milk; It should not be taken by anyone with known hypersensitivity to dairy products or its components. Severe medical events have been associated with epidural administration of Solu-Medrol and Depo-Medrol, including spinal cord infarction, paraplegia, quadriplegia, cortical blindness and stroke. Intramuscular injections should not be administered to those with idiopathic thrombocytopenic purpura. Formulations of Solu-Medrol and Depo-Medrol containing benzyl alcohol are contraindicated for use in premature infants. Exposure of neural tissue to excessive amounts of benzyl alcohol has been associated with toxicity and in rare events has resulted in death.


title: Methylprednisolone

text: There is minimal clinical diagnostic criteria to define the psychic adverse effects (PAE) associated with methylprednisolone use in patients with systemic lupus erythematosus (SLE). The prevalence varies from 1.3 to 62% of adult treated patients. The type and severity of neuropsychiatric symptoms also varies significantly between patients, with 33% of patients reporting mild to moderate PAE and 5-10% reporting severe PAE. Methylprednisolone dose and duration have been implicated in PAE development. 20 mg/day of prednisone (16 mg/day of methylprednisolone) is the threshold dosage for PAE development agreed upon by many studies. Short-term pulse IV therapy at high doses is associated with rapid onset of manic and hypomanic symptoms, whereas long term therapy gives rise to depressive symptoms (suicide attempts infrequent). PAE are reversible with treatment reduction or discontinuation.


title: Methylprednisolone

text: Iatrogenic Cushing's Syndrome is a direct complication of glucocorticoid therapy, and the most common cause of exogenous Cushing's Syndrome. Clinical features of Cushing's Syndrome is inclusive of many adverse effects in glucocorticoid therapy. Traditional symptoms include weight gain, myopathy, osteoporosis, increased risk of infection, hypertension and psychological effect. Fat deposition is centralized on the trunk, in between shoulders ("buffalo hump"), and on the face ("moon face"). Patient education and provider monitoring is the first step in recognizing and diagnosing Iatrogenic Cushing's Syndrome. Exogenous glucocorticoids suppress adrenocorticotropic hormone (ATCH) production, which can be verified by AM biochemical analysis. The onset of side effects varies; neuropsychiatric symptoms can arise within a few hours, while osteoporosis would take months to develop.


title: Methylprednisolone

text: The metabolic effects of taking methylprednisolone involve the continuous breakdown of proteins for gluconeogenesis increase necessity for insulin. This results in hyperlipidemia, weight gain, myopathy that may prompt a patient to cease treatment.


title: Methylprednisolone

text: The Immunodeficiency section tabulates known pathogens of concern in glucocorticoid induced immunodeficiency.


title: Methylprednisolone

text: Osteoporosis is a type of bone disease characterized by a loss of bone density, mass and architecture that leaves a patient susceptible to fractures. The World Health Organization (WHO) defines osteoporosis in caucasian postmenopausal women as a bone mineral density (BMD) and a T-score of -2.5 or less. The prevalence of osteoporosis in patients with SLE varies geographically and some attribute it to BMD and T-score diagnostic appropriateness. British 10.3%, Chinese 21.7%The Canadian Clinical Practice Guidelines and The American College of Rheumatology have switched to using a Z-score as a diagnostic marker for osteoporosis but have failed to find a clinical diagnostic threshold. Additionally, a UK-based study showed that BMD may underrepresent a patient with SLE, as their risk for fractures is 22% higher than the healthy individual.


title: Methylprednisolone

text: Exogenous corticosteroids induce osteoporosis by increasing bone resorption and reducing bone formation. Bone loss can be pronounced within the first few months of initiating methylprednisolone with a steady decrease with chronic use. Trabecular bone loss in the lumbar spine precedes cortical bone loss in the femoral neck.


title: Methylprednisolone

text: Allergic: allergic or hypersensitivity reactions, anaphylactoid reaction, anaphylaxis, and urticaria.


title: Methylprednisolone

text: Cardiovascular: hypertension, congestive heart failure in susceptible patients, premature atherosclerotic disease, arrhythmias, and possible hyperlipidemia.


title: Methylprednisolone

text: Dermatologic: impaired wound healing, petechiae and ecchymoses, thinning of the skin, facial erythema, and increased sweating.


title: Methylprednisolone

text: Endocrine: Cushingoid features, growth suppression in children, secondary adrenocortical and pituitary unresponsiveness, menstrual irregularities, decreased carbohydrate intolerance, and latent diabetes mellitus. In patients with diabetes, increased requirements of insulin or oral hypoglycemic agents.


title: Methylprednisolone

text: Fluid and electrolyte disturbances: sodium retention, fluid retention, potassium loss, hypokalemic alkalosis, or congestive heart failure in susceptible patients.


title: Methylprednisolone

text: Musculoskeletal: muscle weakness, loss of muscle mass, steroid myopathy, osteoporosis, tendon rupture (especially Achilles), vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones.


title: Methylprednisolone

text: Ophthalmic: posterior sub-capsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos.


title: Methylprednisolone

text: Feedback of the exogenous glucocorticoids at the hypothalamic–pituitary–adrenal (HPA) axis inhibits the secretion of the corticotropin-releasing hormone (CRH) and the adrenocorticotropic hormone (ATCH) at the hypothalamus and pituitary glands, respectively. Prolonged suppression leads to inadequate responses to physical and emotional stresses, such as illness and trauma. Suppression of ATCH may result in adrenal hypoplasia or secondary adrenal gland atrophy within 6 weeks of methylprednisolone therapy, leaving a patient at risk for developing life-threatening adrenal insufficiency crisis. Factors that contribute to the extent of HPA axis suppression include steroid hormone potency (type of compound and route of administration), cumulative dose, duration of treatment and concomitant drug use. Any individual who has taken steroid hormones for 2+ weeks is at risk for developing HPA axis suppression. t Systemic methylprednisolone risk has been marked as moderate within the class of synthetic glucocorticoids.


title: Methylprednisolone

text: Consult with your physician prior to discontinuing methylprednisolone for any reason. Abrupt termination of the drug commonly causes transient non-specific symptoms such as loss of appetite, upset stomach, vomiting, drowsiness, confusion, headache, fever, joint and muscle pain, peeling skin, and weight loss. These symptoms can be attributed to steroid withdrawal syndrome, adrenal insufficiency or disease relapse. Those who have been taking methylprednisolone as a long-term treatment may be gradually be tapered off to minimize withdrawal symptoms and potential for relapse. If symptoms are exacerbated, temporarily increasing methylprednisolone dosage has shown clinical relevancy. Studies retesting patients upon methylprednisolone withdrawal, showed persistent adrenal insufficiency, with one study showing 15% after 3 years. However, there was a wide range of prevalence and lack of uniformity in the follow-up timeline.


title: Methylprednisolone

text: All drugs that fall within the class of enzyme inducers increase the clearance and decrease the half-life of methylprednisolone when co-administered. Phenobarbital, phenytoin, rifampin, carbamazepine and barbiturates, increase hepatic enzymes and rate of elimination, thus reducing the immunosuppressive effect of methylprednisolone. Increased dosages may be required to achieve desired effect of methylprednisolone.


title: Methylprednisolone

text: Troleandomycin, ketoconazole, and Clarithromycin inhibit metabolism; and may decrease rate of elimination and increase half-life of methylprednisolone. Dosages should be decreased accordingly to avoid side effects. Another CYP 3A4 inhibitor, grapefruit juice, prolongs half-life of oral methylprednisolone.


title: Methylprednisolone

text: Oral contraceptives inhibit oxidative processes, as highlighted by its ability to decrease methylprednisolone clearance.


title: Methylprednisolone

text: Methylprednisolone is shown to be a substrate of P-glycoprotein; its inhibition is thought to increase methylprednisone absorption and distribution. No clinical relevance has been linked.


title: Methylprednisolone

text: Methylprednisolone and cyclosporin inhibit metabolism and therefore increase the likelihood of experiencing side effects associated with either of the individual drugs. In addition to known individual side effects, convulsions have been reported.


title: Methylprednisolone

text: Methylprednisolone may increase rate of elimination with chronic high dose aspirin. Patient's are susceptible to increased salicylate serum levels or salicylate toxicity upon termination of methylprednisolone. Excessive caution should be taken when prescribing methylprednisolone and aspirin to patients with hypoprothrombinemia.


title: Methylprednisolone

text: Anticoagulants exhibit variable interactions; monitoring coagulation indices is recommended to achieve the desired effect.


title: Methylprednisolone

text: Oral methylprednisolone (Medrol) and its derivatives are a white, odorless crystalline powder. Its solubility ranges from practically insoluble in water, very slightly soluble in ether, sightly soluble in acetone and chloroform to sparingly soluble in alcohol, dioxane and methanol. Methylprednisolone acetate suspension (Depo-Medrol) is a 6-methyl derivative of prednisolone that melts at 215 degrees Celsius with some decomposition. Methylprednisolone sodium succinate (Solu-Medrol) is the sodium succinate ester of methylprednisolone. Contrary to the solubilities above, methylprednisolone sodium succinate is soluble in water and alcohol, slightly soluble in acetone and insoluble in chloroform


title: Methylprednisolone

text: Methylprednisolone, or 6α-methylprednisolone, also known as 11β,17,21-trihydroxy-6α-methylpregna-1,4-diene-3,20-dione, is a synthetic pregnane steroid and a derivative of hydrocortisone (11β,17α,21-trihydroxypregn-4-ene-3,20-dione) and prednisolone (11β,17α,21-trihydroxypregn-1,4-diene-3,20-dione). A variety of methylprednisolone esters with differing characteristics exist and have been marketed for medical use. They include methylprednisolone aceponate (Advantan), methylprednisolone acetate (Depo-Medrol), methylprednisolone succinate (Solu-Medrol), and methylprednisolone suleptanate (Medrosol, Promedrol).


title: Methylprednisolone

text: Synthetic steroids are synthesized from cholic acid and sapogenins obtained from cattle and plants, respectively.


title: Methylprednisolone

text: Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and Food and Drug Administration (FDA) approved in the United States on 2 October 1957. The patent has since expired, and generics are now available. In 2020, it was the 161st most commonly prescribed medication in the United States, with more than 3million prescriptions. Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose.


title: Methylprednisolone

text: Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose.


title: Bankruptcy of Lehman Brothers

text: The bankruptcy of Lehman Brothers on September 15, 2008, was the climax of the subprime mortgage crisis. After the financial services firm was notified of a pending credit downgrade due to its heavy position in subprime mortgages, the Federal Reserve summoned several banks to negotiate financing for its reorganization. These discussions failed, and Lehman filed a Chapter 11 petition that remains the largest bankruptcy filing in U.S. history, involving more than in assets.


title: Bankruptcy of Lehman Brothers

text: The bankruptcy triggered a 4.5% one-day drop in the Dow Jones Industrial Average, then the largest decline since the September 11, 2001, attacks. It signaled a limit to the government's ability to manage the crisis and prompted a general financial panic. Money market mutual funds, a key source of credit, saw mass withdrawal demands to avoid losses, and the interbank lending market tightened, threatening banks with imminent failure. The government and the Federal Reserve system responded with several emergency measures to contain the panic.


title: Bankruptcy of Lehman Brothers

text: As of May 2022, parent company Lehman Brothers Holdings, Inc. remained in liquidation before the Bankruptcy Court for the Southern District of New York. Caretaker offices in the US and abroad have continued to oversee payments to the company's creditors.


title: Bankruptcy of Lehman Brothers

text: Lehman Brothers was one of the first Wall Street firms to move into the business of mortgage origination. In 1997, Lehman bought Colorado-based lender Aurora Loan Services, an Alt-A lender. In 2000, to expand their mortgage origination pipeline, Lehman purchased West Coast subprime mortgage lender BNC Mortgage LLC. Lehman quickly became a force in the subprime market. By 2003 Lehman made $18.2 billion in loans and ranked third in lending. By 2004, this number topped $40 billion. By 2006, Aurora and BNC were lending almost $50 billion per month.


title: Bankruptcy of Lehman Brothers

text: Lehman had morphed into a real estate hedge fund disguised as an investment bank. By 2008, Lehman had assets of $680 billion supported by only $22.5 billion of firm capital. From an equity position, its risky commercial real estate holdings were thirty times greater than capital. In such a highly leveraged structure, a three- to five-percent decline in real estate values would wipe out all capital.


title: Bankruptcy of Lehman Brothers

text: Lehman borrowed significant amounts to fund its investing in the years leading to its bankruptcy in 2008, an intricate process known as leveraging or gearing. A significant portion of this investment was in housing-related assets, making it vulnerable to a downturn in that market. One measure of this risk-taking was its leverage ratio, a measure of the ratio of assets to owners equity, which increased from approximately 24:1 in 2003 to 31:1 by 2007. While generating tremendous profits during the boom, this vulnerable position meant that just a 3–4% decline in the value of its assets would entirely eliminate its book value of equity. Investment banks such as Lehman were not subject to the same regulations applied to depository banks to restrict their risk-taking.


title: Bankruptcy of Lehman Brothers

text: In August 2007, Lehman closed its subprime lender, BNC Mortgage, eliminating 1,200 positions in 23 locations, and took a $25-million after-tax charge and a $27-million reduction in goodwill. The firm said that poor market conditions in the mortgage space "necessitated a substantial reduction in its resources and capacity in the subprime space".


title: Bankruptcy of Lehman Brothers

text: In 2008, Lehman faced an unprecedented loss due to the continuing subprime mortgage crisis. Lehman's loss resulted from having held onto large positions in subprime and other lower-rated mortgage tranches when securitizing the underlying mortgages. Whether Lehman did this because it was simply unable to sell the lower-rated bonds, or made a conscious decision to hold them, is unclear. In any event, huge losses accrued in lower-rated mortgage-backed securities throughout 2008. In the second fiscal quarter, Lehman reported losses of $2.8 billion and decided to raise $6 billion in additional capital by offering new shares. In the first half of 2008 alone, Lehman stock lost 73% of its value as the credit market continued to tighten. In August 2008, Lehman reported that it intended to release 6% of its work force, 1,500 people, just ahead of its third-quarter-reporting deadline in September.


title: Bankruptcy of Lehman Brothers

text: On August 22, shares in Lehman closed up 5% (16% for the week) on reports that the state-controlled Korea Development Bank was considering buying Lehman. Most of those gains were quickly eroded as news emerged that Korea Development Bank was "facing difficulties pleasing regulators and attracting partners for the deal." It culminated on September 9, when Lehman's shares plunged 45% to $7.79, after it was reported that the state-run South Korean firm had put talks on hold.


title: Bankruptcy of Lehman Brothers

text: Investor confidence continued to erode as Lehman's stock lost roughly half its value and pushed the S&P 500 down 3.4% on September 9. The Dow Jones lost nearly 300 points the same day, on investors' concerns about the security of the bank. The U.S. government did not announce any plans to assist with any possible financial crisis that emerged at Lehman.


title: Bankruptcy of Lehman Brothers

text: On September 10, Lehman announced a loss of $3.9 billion and their intent to sell off a majority stake in their investment-management business, which included Neuberger Berman. The stock slid 7% that day.


title: Bankruptcy of Lehman Brothers

text: On September 12, Timothy F. Geithner, then president of the Federal Reserve Bank of New York, called a meeting on the future of Lehman, which included the possibility of an emergency liquidation of its assets. Bankers representing all the major Wall Street firms were in attendance. The meeting goal was to find a private solution in rescuing Lehman and extinguish the flame of the global financial crisis. Lehman reported that it had been in talks with Bank of America and Barclays for the company's possible sale. "The New York Times" reported on September 14, 2008, that Barclays had ended its bid to purchase all or part of Lehman and a deal to rescue the bank from liquidation collapsed. It emerged subsequently that a deal had been vetoed by the Bank of England and the UK's Financial Services Authority. Leaders of major Wall Street banks continued to meet late that day to prevent the bank's rapid failure. Bank of America's rumored involvement also appeared to end as federal regulators resisted its request for government involvement in Lehman's sale. By Sunday, September 14, after the Barclays deal fell through, the news of impending doom swept through Lehman, and many employees arrived at the headquarters to clean out their offices. By Sunday afternoon, the government summoned Harvey Miller of Weil, Gotshal & Manges to file for bankruptcy before the markets opened on Monday.


title: Bankruptcy of Lehman Brothers

text: Lehman Brothers filed for Chapter 11 bankruptcy protection on Monday, September 15, 2008. According to Bloomberg, reports filed with the U.S. Bankruptcy Court, Southern District of New York (Manhattan) on September 16 indicated that JPMorgan Chase & Co. provided Lehman Brothers with a total of $138 billion in "Federal Reserve-backed advances". The "Federal Reserve-backed advances" as provided by JPMorgan Chase were for $87 billion on September 15 and $51 billion on September 16.


title: Bankruptcy of Lehman Brothers

text: The filing remains the largest bankruptcy filing in U.S. history, with Lehman holding over $600 billion in assets.


title: Bankruptcy of Lehman Brothers

text: On September 22, 2008, a revised proposal to sell the brokerage part of Lehman Brothers holdings of the deal, was put before the bankruptcy court, with a $1.3666 billion (£700 million) plan for Barclays to acquire the core business of Lehman Brothers (mainly Lehman's $960 million Midtown Manhattan office skyscraper), was approved. Manhattan court bankruptcy Judge James Peck, after a seven-hour hearing, ruled: "I have to approve this transaction because it is the only available transaction. Lehman Brothers became a victim, in effect the only true icon to fall in a tsunami that has befallen the credit markets. This is the most momentous bankruptcy hearing I've ever sat through. It can never be deemed precedent for future cases. It's hard for me to imagine a similar emergency."


title: Bankruptcy of Lehman Brothers

text: Luc Despins, the creditors committee counsel, said: "The reason we're not objecting is really based on the lack of a viable alternative. We did not support the transaction because there had not been enough time to properly review it." In the amended agreement, Barclays would absorb $47.4 billion in securities and assume $45.5 billion in trading liabilities. Lehman's attorney Harvey R. Miller of Weil, Gotshal & Manges, said "the purchase price for the real estate components of the deal would be $1.29 billion, including $960 million for Lehman's New York headquarters and $330 million for two New Jersey data centers. Further, Barclays will not acquire Lehman's Eagle Energy unit, but will have entities known as Lehman Brothers Canada Inc, Lehman Brothers Sudamerica, Lehman Brothers Uruguay and its Private Investment Management business for high-net-worth individuals. Finally, Lehman will retain $20 billion of securities assets in Lehman Brothers Inc that are not being transferred to Barclays. Barclays had a potential liability of $2.5 billion to be paid as severance, if it chooses not to retain some Lehman employees beyond the guaranteed 90 days.


title: Bankruptcy of Lehman Brothers

text: On September 22, 2008, Nomura Holdings, Inc. announced it agreed to acquire Lehman Brothers' franchise in the Asia Pacific region including Japan, Hong Kong and Australia. The following day, Nomura announced its intentions to acquire Lehman Brothers' investment banking and equities businesses in Europe and the Middle East. A few weeks later it was announced that conditions to the deal had been met, and the deal became legally effective on Monday, October 13. In 2007, non-US subsidiaries of Lehman Brothers were responsible for over 50% of global revenue produced.


title: Bankruptcy of Lehman Brothers

text: The Dow Jones closed down just over 500 points (−4.4%) on September 15, 2008, at the time the largest drop by points in a single day since the days following the attacks on September 11, 2001. This drop was exceeded by a 6.98% plunge on September 29, 2008.


title: Bankruptcy of Lehman Brothers

text: Lehman's bankruptcy was expected to cause some depreciation in the price of commercial real estate. The prospect for Lehman's $4.3 billion in mortgage securities getting liquidated sparked a selloff in the commercial mortgage-backed securities (CMBS) market. Additional pressure to sell securities in commercial real estate was feared as Lehman got closer to liquidating its assets. Apartment-building investors were also expected to feel pressure to sell as Lehman unloaded its debt and equity pieces of the $22 billion purchase of Archstone, the third-largest United States real estate investment trust (REIT). Archstone's core business was the ownership and management of residential apartment buildings in major metropolitan areas of the United States. Jeffrey Spector, a real-estate analyst at UBS, said that in markets with apartment buildings that compete with Archstone, "there is no question that if you need to sell assets, you will try to get ahead" of the Lehman selloff, adding "Every day that goes by there will be more pressure on pricing."


title: Bankruptcy of Lehman Brothers

text: Several money funds and institutional cash funds had significant exposure to Lehman with the institutional cash fund run by The Bank of New York Mellon and the Reserve Primary Fund, a money market fund, both falling below $1 per share, called "breaking the buck", following losses on their holdings of Lehman assets. In a statement The Bank of New York Mellon said its fund had isolated the Lehman assets in a separate structure. It said the assets accounted for 1.13% of its fund. The Primary Reserve Fund owned $785 million or 1.2 percent of its holdings in Lehman commercial paper. The drop in the Primary Reserve Fund was the first time since 1994 that a money-market fund had dropped below the $1-per-share level.


title: Bankruptcy of Lehman Brothers

text: On Monday, September 15, 2008, the market staged a run on AIG with shares plummeting 61 percent. Shareholders also fled from Goldman Sachs and Morgan Stanley. Two weeks later, the Fed agreed to give the bank holding company status which provided vital access to the Fed discount window.


title: Bankruptcy of Lehman Brothers

text: Putnam Investments, a unit of Canada's Great-West Lifeco, shut a $12.3 billion money-market fund as it faced "significant redemption pressure" on September 17, 2008. Evergreen Investments said its parent Wachovia Corporation would "support" three Evergreen money-market funds to prevent their shares from falling. This move to cover $494 million of Lehman assets in the funds also raised fears about Wachovia's ability to raise capital.


title: Bankruptcy of Lehman Brothers

text: Close to 100 hedge funds used Lehman as their prime broker and relied largely on the firm for financing. In an attempt to meet their own credit needs, Lehman Brothers International routinely re-hypothecated the assets of their hedge funds clients that utilized their prime brokerage services. Lehman Brothers International held close to 40 billion dollars of clients assets when it filed for Chapter 11 Bankruptcy. Of this, 22 billion had been re-hypothecated. As administrators took charge of the London business and the U.S. holding company filed for bankruptcy, positions held by those hedge funds at Lehman were frozen. As a result, the hedge funds were forced to de-lever and sit on large cash balances, inhibiting chances at further growth. This in turn created further market dislocation and overall systemic risk, resulting in a 737 billion dollar decline in collateral outstanding in the securities lending market.


title: Bankruptcy of Lehman Brothers

text: In Japan, banks and insurers announced a combined 249 billion yen ($2.4 billion) in potential losses tied to the Lehman shock. Mizuho Trust & Banking cut its profit forecast by more than half, citing 11.8 billion yen in losses on bonds and loans linked to Lehman. The Bank of Japan Governor Masaaki Shirakawa said, "Most lending to Lehman Brothers was made by major Japanese banks, and their possible losses seem to be within the levels that can be covered by their profits," adding, "There is no concern that the latest events will threaten the stability of Japan's financial system." During bankruptcy proceedings a lawyer from The Royal Bank of Scotland Group said the company was facing between $1.5 billion and $1.8 billion in claims against Lehman partially based on an unsecured guarantee from Lehman and connected to trading losses with Lehman subsidiaries, Martin Bienenstock.


title: Bankruptcy of Lehman Brothers

text: Lehman was a counterparty to mortgage financier Freddie Mac in unsecured lending transactions that matured on September 15, 2008. Freddie said it had not received principal payments of $1.2 billion plus accrued interest. Freddie said it had further potential exposure to Lehman of about $400 million related to the servicing of single-family home loans, including repurchasing obligations. Freddie also said it "does not know whether and to what extent it will sustain a loss relating to the transactions" and warned that "actual losses could materially exceed current estimates." Freddie was still in the process of evaluating its exposure to Lehman and its affiliates under other business relationships.


title: Bankruptcy of Lehman Brothers

text: After Constellation Energy was reported to have exposure to Lehman, its stock went down 56% in the first day of trading having started at $67.87. The massive drop in stocks led to the New York Stock Exchange halting trade of Constellation. The next day, as the stock plummeted as low as $13 per share, Constellation announced it was hiring Morgan Stanley and UBS to advise it on "strategic alternatives", suggesting a buyout. While rumors suggested French power company Électricité de France would buy the company or increase its stake, Constellation ultimately agreed to a buyout by MidAmerican Energy, part of Berkshire Hathaway (headed by billionaire Warren Buffett).


title: Bankruptcy of Lehman Brothers

text: The Federal Agricultural Mortgage Corporation or Farmer Mac said it would have to write off $52.4 million in Lehman debt in the form of senior debt securities it owned as a result of the bankruptcy. Farmer Mac said it might not be in compliance with its minimum capital requirements at the end of September.


title: Bankruptcy of Lehman Brothers

text: In Hong Kong more than 43,700 individuals in the city had invested in HK$15.7 billion of "guaranteed mini-bonds" (迷你債券) from Lehman. Many claim that banks and brokers mis-sold them as low-risk. Conversely, bankers note that minibonds are indeed low-risk instruments since they were backed by Lehman Brothers, which until just months before its collapse was a venerable member of Wall Street with high credit and investment ratings. The default of Lehman Brothers was a low probability event, which was totally unexpected. Indeed, many banks accepted minibonds as collateral for loans and credit facilities. Another HK$3 billion was invested in similar like derivatives. The Hong Kong government proposed a plan to buy back the investments at their current estimated value, which would allow investors to partially recover some of their loss by the end of the year. HK chief executive Donald Tsang insisted the local banks respond swiftly to the government buy-back proposal as the Monetary Authority received more than 16,000 complaints. On October 17, He Guangbe, chairman of the Hong Kong Association of Banks, agreed to buy back the bonds, which were priced using an agreed upon methodology based on its estimated current value. This episode had deep repercussions on the banking industry, where misguided investor sentiments became hostile to both wealth management products as well as the banking industry as a whole. Under intense pressure from the public, all political parties came out in support of the investors, further fanning distrust towards the banking industry.


title: Bankruptcy of Lehman Brothers

text: Neuberger Berman Inc., through its subsidiaries, primarily Neuberger Berman, LLC, is an investment-advisory firm founded in 1939 by Roy R. Neuberger and Robert Berman, to manage money for high-net-worth individuals. In the decades that followed, the firm's growth mirrored that of the asset-management industry as a whole. In 1950, it introduced one of the first no-load mutual funds in the United States, the Guardian Fund, and also began to manage the assets of pension plans and other institutions. Historically known for its value-investing style, in the 1990s the firm began to diversify its competencies to include additional value and growth investing, across the entire capitalization spectrum, as well as new investment categories, such as international, real-estate investment trusts and high-yield investments. In addition, with the creation of a nationally and several state-chartered trust companies, the firm became able to offer trust and fiduciary services. In 2016, the firm had approximately $246 billion in assets under management.


title: Bankruptcy of Lehman Brothers

text: In October 1999, the firm conducted an initial public offering of its shares and commenced trading on the New York Stock Exchange, under the ticker symbol "NEU". In July 2003, shortly after the retired Mr. Neuberger's 100th birthday, the company announced that it was in merger discussions with Lehman Brothers Holdings Inc. These discussions ultimately resulted in the firm's acquisition by Lehman on October 31, 2003, for approximately $2.63 billion in cash and securities.


title: Bankruptcy of Lehman Brothers

text: On November 20, 2006, Lehman announced its Neuberger Berman subsidiary would acquire H. A. Schupf & Co., a money-management firm targeted at wealthy individuals. Its $2.5 billion of assets would join Neuberger's $50 billion in high-net-worth client assets under management.


title: Bankruptcy of Lehman Brothers

text: An article in The Wall Street Journal on September 15, 2008, announcing that Lehman Brothers Holdings filed for Chapter 11 bankruptcy protection, quoted Lehman officials regarding Neuberger Berman: ""Neuberger Berman LLC and Lehman Brothers Asset Management will continue to conduct business as usual and will not be subject to the bankruptcy case of the parent company, and its portfolio management, research and operating functions remain intact. In addition, fully paid securities of customers of Neuberger Berman are segregated from the assets of Lehman Brothers and aren't subject to the claims of Lehman Brothers Holdings' creditors, Lehman said.""


title: Bankruptcy of Lehman Brothers

text: Just before the collapse of Lehman Brothers, executives at Neuberger Berman sent e-mail memos suggesting, among other things, that the Lehman Brothers' top people forgo multimillion-dollar bonuses to "send a strong message to both employees and investors that management is not shirking accountability for recent performance".


title: Bankruptcy of Lehman Brothers

text: Lehman Brothers Investment Management Director George Herbert Walker IV dismissed the proposal, going so far as to actually apologize to other members of the Lehman Brothers executive committee for the idea of bonus reduction having been suggested. He wrote, "Sorry team. I am not sure what's in the water at Neuberger Berman. I'm embarrassed and I apologize."


title: Bankruptcy of Lehman Brothers

text: Richard Fuld, head of Lehman Brothers, faced questioning from the U.S. House of Representatives' Committee on Oversight and Government Reform. Rep. Henry Waxman (D-CA) asked: "Your company is now bankrupt, our economy is in crisis, but you get to keep $480 million (£276 million). I have a very basic question for you, is this fair?" Fuld said that he had in fact taken about $300 million (£173 million) in pay and bonuses over the past eight years. Despite Fuld's defense on his high pay, Lehman Brothers executive pay was reported to have increased significantly before filing for bankruptcy. On October 17, 2008, CNBC reported that several Lehman executives, including Richard Fuld, had been subpoenaed in a case relating to securities fraud.


title: Bankruptcy of Lehman Brothers

text: In March 2010, the report of Anton R. Valukas, the Bankruptcy Examiner, drew attention to the use of Repo 105 transactions to boost the bank's apparent financial position around the date of the year-end balance sheet. The New York attorney general Andrew Cuomo later filed charges against the bank's auditors Ernst & Young in December 2010, alleging that the firm "substantially assisted... a massive accounting fraud" by approving the accounting treatment.


title: Bankruptcy of Lehman Brothers

text: On April 12, 2010, a story in "The New York Times" revealed that Lehman had used a small company, Hudson Castle, to move a number of transactions and assets off Lehman's books as a means of manipulating accounting numbers of Lehman's finances and risks. One Lehman executive described Hudson Castle as an "alter ego" of Lehman. According to the story, Lehman owned one quarter of Hudson; Hudson's board was controlled by Lehman, most Hudson staff members were former Lehman employees.


title: Bankruptcy of Lehman Brothers

text: On February 22, 2011, Judge James M. Peck of the U.S. Bankruptcy Court in the Southern District of New York rejected claims by lawyers for the Lehman estate that Barclays had improperly reaped a windfall from the section 363 sale. "The sale process may have been imperfect, but it was still adequate under the exceptional circumstances of Lehman Week."


title: Andrew Shue

text: Andrew Eppley Shue (born February 20, 1967) is an American actor, known for his role as Billy Campbell on the television series "Melrose Place" (1992–1999). Shue played soccer professionally for several years. He co-founded and served on the board of directors of the global non-profit organization Do Something, and co-founded the social networking website CafeMom.


title: Andrew Shue

text: Shue was born in Wilmington, Delaware. His mother, Anne Brewster (née Wells; born 1938), is a bank executive who was the vice president of the private division of the Chemical Bank Corporation. His father, James William Shue (born 1936 – died May 24, 2013), was a lawyer and real estate developer who was the president of the International Food and Beverage Corporation and was active in Republican politics, having once unsuccessfully run for the U.S. Congress in New Jersey. His mother was a descendant of Pilgrim leader William Brewster and his father was of German ancestry, from Pennsylvania.


title: Andrew Shue

text: Shue's sister Elisabeth is an actress; in three of his early uncredited film appearances, he appeared with her in "The Karate Kid", "Cocktail" and "Adventures in Babysitting".


title: Andrew Shue

text: Shue attended Columbia High School in Maplewood, New Jersey. Along with his sister, he was inducted into the CHS Hall of fame in 1994. At Dartmouth College, as he was in high school, Shue was a Regional All America soccer player and spent a winter studying and playing soccer in Glasgow, Scotland for Queen's Park FC. Shue received his B.A. in history from Dartmouth in 1989. After graduating, he visited Zimbabwe, where he simultaneously played soccer and taught high school math at Founders High School.


title: Andrew Shue

text: In May 1992, Shue was cast to play the role of Billy Campbell on the Aaron Spelling soap opera "Melrose Place". He starred opposite Courtney Thorne-Smith, whom he later dated. Shue stayed on the show for six years. During this time, he appeared as an abusive husband in the Francis Ford Coppola film "The Rainmaker", starring Matt Damon and Claire Danes.


title: Andrew Shue

text: A 1996 commercial for "SportsCenter" on ESPN has Shue being traded for former "SportsCenter" anchor Charley Steiner, where Steiner takes his position on "Melrose Place" and Shue takes his on "SportsCenter".


title: Andrew Shue

text: He worked on the 2007 feature film, "Gracie", with his sister Elisabeth, his brother John, and his brother-in-law, Davis Guggenheim, the Oscar-winning director of "An Inconvenient Truth". Shue co-produced the film and also appeared in a minor role. It pays tribute to the Shue siblings' elder brother Will, who died in an accident in 1988. The story is loosely based on Elisabeth's childhood, when she was the only girl playing on an all-boys soccer team.


title: Andrew Shue

text: During his time in Zimbabwe, Shue played for Bulawayo Highlanders. That season, the Highlanders won both Zimbabwe Premier Soccer League and CBZ Cup titles. At the time, Shue was the only white player in the Zimbabwe Premier Soccer League. In September 1993, he played one game with Los Angeles United of the Continental Indoor Soccer League. In July 1994, he played two games for Anaheim Splash. In 1996, while still on "Melrose Place", Shue played for the Los Angeles Galaxy of Major League Soccer, recording one assist in five games. He spent the entire 1997 season on injured reserve.


title: Andrew Shue

text: Along with his childhood best friend Michael Sanchez, Shue co-founded DoSomething. He now sits on the board of directors.