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The Merv Griffin Show

The Merv Griffin Show is an American television talk show starring Merv Griffin. The series ran from October 1, 1962 to March 29, 1963 on NBC, May 1965 to August 15, 1969 in first-run syndication, from August 18, 1969 to February 11, 1972 at 11:30 PM ET weeknights on CBS and again in first-run syndication from February 14, 1972 to September 5, 1986. After a short run on NBC from October 1962 to March 1963, Merv Griffin launched a syndicated version of his talk show produced by Westinghouse Broadcasting, which made its debut in May 1965. Intended as a nighttime companion to The Mike Douglas Show and succeeding Steve Allen and Regis Philbin in the time slot, this version of the Griffin program aired in multiple time slots throughout North America. Stations had the option of carrying a 90-minute version. Griffin's announcer-sidekick was the veteran British character actor Arthur Treacher, his mentor. Treacher would introduce Griffin with the phrase: "...and now, here's the dear boy himself, Meeeer-vyn!" after reading off the list of guests for that evening's show.

Seeing his strong ratings, CBS offered him a network series opposite the powerhouse Tonight Show, his program moved there in the fall of 1969, with his debut guest lineup consisting of Hedy Lamarr, Ted Sorensen, Leslie Uggams, Moms Mabley, Woody Allen. Although the series did well enough to force the cancellation of another Carson competitor, ABC's The Joey Bishop Show, it was unable to make much of a dent in Carson's ratings. Furthermore, the network was uncomfortable with the guests Griffin wanted, who spoke out against the Vietnam War and on other taboo topics; when political activist Abbie Hoffman was Griffin's guest in April 1970, CBS blurred the video of Hoffman so viewers at home would not see his trademark American flag pattern shirt though other guests had worn the same shirt in the past and Pat Boone appeared in an automobile commercial on that broadcast wearing a similar flag-motif shirt. That same year, Griffin relocated his show from New York to Los Angeles, but without sidekick Arthur Treacher, who told him "at my age, I don't want to move to someplace that shakes!".

From that point on, Griffin would do the announcing himself, walk on stage with the phrase: "And now... here I come!" However, Griffin's show continued to rank in second place behind Carson after the move. By early 1972, sensing that his time at CBS was ending, tired of the restrictions imposed by the network, Griffin secretly signed a contract with Metromedia and its production arm, Metromedia Producers Corporation to continue his program in syndication soon as CBS canceled Griffin's show. Within a few months, Griffin was fired by CBS, his new show began the following Monday and proved to be more successful than its network counterpart. This version returned Merv to late night time slots. Metromedia gave Griffin prime time clearances on the company's group of independent stations, which included outlets in New York, Los Angeles, Minneapolis–Saint Paul and Washington, D. C. Beginning in 1981, The Merv Griffin Show was cut back to one hour in order to accommodate stations who preferred that length over the 90-minute version.

King World Productions took over syndication of the program in 1984 as part of a wider, blanket deal with Merv Griffin Enterprises which included the launch of the nighttime version of Wheel of Fortune, a revival of Jeopardy!. Though MPC no longer syndicated the program, Metromedia's independent stations continued to carry it until they were sold in early 1986 to News Corporation and 20th Century Fox, who used the stations as the nucleus of the Fox Broadcasting Company; as Fox was setting up its own late-night talk show, The Late Show Starring Joan Rivers, the former Metromedia stations dropped the show soon thereafter. The show was canceled altogether that year, aired its final episode on September 5, 1986. Griffin's conversational style created the perfect atmosphere for conducting intelligent interviews that could be serious with some and light-hearted with others. Rather than interview a guest for a cursory 5- or 6-minute segment, Merv preferred lengthy, in-depth discussions with many stretching out past 30 minutes.

In addition, Griffin sometimes dedicated an entire show to a single person or topic, allowing for greater exploration of his guests’ personality and thoughts. Griffin’s idea of the perfect show was to have as many diverse guests as possible, from entertainers to scientists, Hollywood glamour to Vegas variety, from comedians to political leaders. A perfect example lies in an episode from September 1965 which featured the zany comedian Phyllis Diller followed by an interview with Capt. Mitsuo Fuchida, the Japanese navy officer who planned and led the attack on Pearl Harbor in 1941— a unique moment in television history. For over a quarter of a century, more than 25,000 guests appeared on The Merv Griffin Show including numerous significant cultural, political and musical icons of the 1960s, 1970s and 1980s. Four U. S. Presidents -- Richard Nixon, Gerald Ford, Jimmy Carter and Ronald Reagan appeared, as did Dr. Martin Luther King, Rosa Parks, Dr. Jonas Salk and Robert F. Kennedy. Legendary actors and directors who appeared on the program include Orson Welles, John Wayne, Judy Garland, Doris Day, Robert De Niro, Tom Cruise, Sophia Loren, George Clooney, Tom Hanks, Gene Wilder, Francis Ford Coppola, Dustin Hoffman, Clint Eastwood and Grace Kel

Chronic periodontitis

Chronic periodontitis is one of the seven categories of periodontitis as defined by the American Academy of Periodontology 1999 classification system. Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues, caused by the accumulation of profuse amounts of dental plaque. Periodontitis begins as gingivitis and can progress onto chronic and subsequent aggressive periodontitis according to the 1999 classification. Diagnosing chronic periodontitis is important in its early stages to prevent severe and irreversable damage to the protective and supportive structures of the tooth. However, due to chronic periodontitis being a painless progressing disease, few patients will seek dental care in the early stages. Mild to moderate chronic periodontitis can be managed by proper mechanical removal of the biofilm and calculus subgingivally. Full and effective oral hygiene and regular 3 monthly periodontal checkups are important for maintaining the stability of the disease.

Chronic periodontitis is prevalent in seniors worldwide. In the US around 35% of adults are affected; the cumulative effects of alveolar bone loss, attachment loss and pocket formation is more apparent with an increase in age. Age is related to the incidence of periodontal destruction: "...in a well-maintained population who practises oral home care and has regular check-ups, the incidence of incipient periodontal destruction increases with age, the highest rate occurs between 50 and 60 years, gingival recession is the predominant lesion before 40 years, while periodontal pocketing is the principal mode of destruction between 50 and 60 years of age."There are a variety of periodontal risk factors which can affect the prevalence, rate and severity of the disease progression. Major risk factors include lack of oral hygiene with inadequate plaque biofilm control. There is a slow to moderate rate of disease progression but the patient may have periods of rapid progression. Chronic periodontitis can be associated with local predisposing factors.

The disease may be modified by and be associated with systemic diseases It can be modified by factors other than systemic disease such as smoking and emotional stress and depression. Care should be taken however, when diagnosing a patient who smokes as smoking can alter some of the results of an examination. In smokers, the gingiva are pale and fibrous and tend to bleed less while being probed due to the effect of nicotine on the vasculature by vasoconstricting them. Thus, a lowered response is produced and this explains why incorrect data can be gained. There is an increase in supragingival calculus alongside visible nicotine staining; the anterior dentition have recession and maxillary anterior and palatal surfaces are more adversely affected. Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament.

Major drivers of this aggressive tissue destruction are matrix metalloproteinases and other osteoclast-derived enzymes. At least two mechanisms of the microbiology of periodontitis have been described: the specific plaque hypothesis and the non-specific plaque hypothesis. Consensus is that neither view is correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque; this is called the ecological plaque hypothesis. The disease is associated with a variable microbial pattern. Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in chronic periodontitis. Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, Eikenella corrodens may play a role in chronic periodontitis. In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed before they seek treatment.

Symptoms may include the following: Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food Gum swelling that reoccurs Halitosis, or bad breath, a persistent metallic taste in the mouth Gingival recession, resulting in apparent lengthening of teeth. Deep pockets between the teeth and the gums Loose teeth, in the stages Drifting of incisorsGingival inflammation and bone destruction are painless. Patients sometimes assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing chronic periodontitis in that patient. Subgingival calculus is a frequent finding as well as supragingival calculus due to the bacteria migrating apically and the combined effect of the host response system of the body. Chronic periodontitis is one of the seven destructive periodontal diseases as listed in the 1999 classification. Not every case of gingivitis will progress onto chronic periodontitis, but all chronic perodontitis results from gingivits.

Therefore it is important to control the first step.

Berkeley Lake, Georgia

Berkeley Lake is a city in Gwinnett County, United States. It is an affluent northern suburb of Atlanta. From its 1956 origins as a summer retreat, Berkeley Lake has grown into a thriving community centered on its 88-acre namesake lake; as of the 2010 census, the city had a population of 1,574. It has been named a Tree City USA for 18 years. Berkeley Lake residents are a mix of entrepreneurs, corporate executives, other professionals. There is a large number of artists and writers. With a median household income of $131,944, Berkeley Lake is the most affluent town in the state of Georgia. Berkeley Lake is in western Gwinnett County, bordered by Duluth to the east, Peachtree Corners to the south and west, Johns Creek to the north; the northern boundary of the city follows the Chattahoochee River, the Fulton County line. Peachtree Industrial Boulevard is the main road through the city; the community consists of several subdivisions around an 88-acre private lake. According to the United States Census Bureau, the city has a total area of 1.2 square miles, of which 1.1 square miles is land and 0.1 square miles, or 10.14%, is water.

As of the census of 2010, there were 1,574 people, 472 households, 474 families residing in the city. The population density was 1,312 people per square mile. There were 606 housing units at an average density of 505 per square mile; the racial makeup of the city was 75.5% White, 5.7% African American, 0.1% Native American, 14.3% Asian, 1.3% from other races, 3.1% from two or more races. Hispanic or Latino of any race were 3.6% of the population. There were 572 households out of which 37.2% had children under the age of 18 living with them, 75.7% were married couples living together, 5.6% had a female householder with no husband present, 17.1% were non-families. 13.3% of all households were made up of individuals and 5.8% had someone living alone, 65 years of age or older. The average household size was 2.75 and the average family size was 3.04. In the city, the population was spread out with 25.3% under the age of 18, 3.9% from 18 to 24, 18.7% from 25 to 44, 40.4% from 45 to 64, 11.7% who were 65 years of age or older.

The median age was 46.0 years. For every 100 females, there were 98.5 males. For every 100 females age 18 and over, there were 92.6 males. According to the 2015 American Community Survey, the median income for a household in the city was $118,571, the median income for a family was $130,100. Males had a median income of $104,643 versus $65,417 for females; the per capita income for the city was $51,773. About 3.3% of families and 3.0% of the population were below the poverty line, including 1.9% of those under age 18 and 7.9% of those age 65 or over. A number of collector roads distribute traffic around both incorporated and unincorporated areas of the city. Gwinnett County Transit serves the city; the Loop Trail Western Gwinnett Bikeway The majority of lands in the city limits was developed by Frank Coggins in the late 1940s. The dam, constructed in 1948, is one of the largest earthen dams in the state; the city's namesake, Lake Berkeley, was named after Mr. Coggins' Berkeley Blue Granite Quarries in Elberton.

In 1950 the Berkeley Lake "subdivision," which included five reserved Free Pass and Repass tracts and the residential and fishing lots around the lake, was laid out. In 1952, Calvin and Kate Parsons, along with John and Dorothy Bagwell, purchased the Berkeley Realty & Investment Company and its 700-acre property. For many years, Berkeley Lake was a summer retreat, with an assortment of fishing cottages mingling with a growing number of permanent homes; the health of the lake was guarded by a small, but tenacious, core of residents, each lending their expertise and time. In 1953, some 25 property owners formed the Lake Berkeley Civic Association. Besides zoning and developmental control, there were important needs such as electricity, "an all year road" around the lake; this need for benefits that an incorporated city could help secure brought about the creation of its charter, approved by the General Assembly of Georgia on March 6, 1956. A new municipality to be known as the City of Berkeley Lake was created in Gwinnett County.

Over the years since the city's incorporation, a number of ordinances have been passed to protect the character and tranquility of the community. In addition, a comprehensive master plan for future land use and growth was adopted. Since 1994, five new subdivisions have been added to nearly complete the development of all the land within the city limits. Only two tracts of over 10 acres remain. In November 1996, residents supported a referendum for the issuance of a bond to be used to purchase one of these tracts 63 acres of undeveloped forest land; this property, which provides both buffer and greenspace, was acquired by the city in December 1996. In 2009, the city received the Lake Berkeley Dam was damaged; the lake was subsequently drained and, with the help of FEMA, repaired. The Lake Berkeley Dam repairs were completed in 2013, the lake returned to full pool in 2014. Berkeley Lake residents are zoned to Duluth cluster schools in the Gwinnett County Public Schools system: Berkeley Lake Elementary, Duluth Middle, Duluth High School.

City of Berkeley Lake official website Berkeley Lake community website

Siham Alawami

Siham Alawami is a Qatari woman known for her documentaries of Arab culture in Austria. She has worked with legendary U. S. boxer, Muhammad Ali. Qatari-born, left the Middle East after completing high school to study further in Austria, she graduated from Webster University Vienna with Master's degrees in European Studies and European Law. Alawam developed TV programs and campaigns to promote the City of Vienna and its relations with the Gulf countries, as well as creating an understanding among the youth of Vienna. Alawami started as a PR specialist for the intergovernmental organization, OPEC, in Austria where she spent over 30 years and organized 30 Viennese Balls in Dubai, Abu Dhabi and Oman, the last of, in 1996; as part of her role at OPEC she was responsible for briefing NATO on OPEC's goals and mission. Alawami has worked as a print and television journalist and has produced and presented various TV programs in Arabic and German. In 1977, Alawami worked as a private secretary for boxing legend Muhammad Ali at his Deer Lake Training Camp.

The European Society of Communication and Education awarded Alawami the ERASMUS Seal of Approval for four of her TV programs: 2008 ‘Vienna-Mozart and Um Kulthom’ 2009 ‘Salam Islam’ 2010 ‘Vienna and Arabs - Culture and Business’ 2011 ‘The Qatar Philharmonic Orchestra in Vienna’ Alawami returned to Qatar, joining the International Centre for Sport Security in August 2011, working directly with its President, Mohammed Hanzab. The ICSS is an international non-profit organisation with its headquarters in Qatar, it was established in 2010, aiming to share expertise in the fields of safety and integrity at major international sporting events. The organisation's main roles include advisory and research working with organising committees, bidding nations, infrastructure owners, sport associations and clubs; the ICSS organises the annual conference, "Securing Sport", held in Doha, Qatar of which Alawami is a driving force. Http://www.theicss.org The International Centre for Sport Security page

2013–14 Virginia Cavaliers men's basketball team

The 2013–14 Virginia Cavaliers men's basketball team represented the University of Virginia during the 2013–14 NCAA Division I men's basketball season. The team was led by head coach Tony Bennett, in his fifth season, played their home games at John Paul Jones Arena as members of the Atlantic Coast Conference; the 2013–14 season was one of the most successful in UVa's 109-year basketball history. The Cavaliers won only their second outright ACC regular season title, with a 16–2 conference record, as well as only their second ACC Tournament title, they won 30 games for only the second time in school history and finished third in the final AP Poll—their highest final national ranking in 30 years. On March 16, 2014, the Cavaliers received a #1 seed in the NCAA Tournament. In the NCAA Tournament, they defeated Coastal Carolina and Memphis to advance to the Sweet Sixteen, where they lost to Michigan State

CD97

Cluster of differentiation 97 is a protein known as BL-Ac encoded by the ADGRE5 gene. CD97 is a member of the adhesion G protein-coupled receptor family. Adhesion GPCRs are characterized by an extended extracellular region possessing N-terminal protein modules, linked to a TM7 region via a domain known as the GPCR-Autoproteolysis INducing domain. CD97 is expressed on, among others, hematopoietic stem and progenitor cells, immune cells, epithelial cells, muscle cells as well as their malignant counterparts. In the case of CD97 the N-terminal domains consist of alternatively spliced epidermal growth factor -like domains. Alternative splicing has been observed for this gene and three variants have been found; the N-terminal fragment of CD97 contains 3-5 EGF-like domains in human and 3-4 EGF-like domains in mice. Decay accelerating factor, a regulatory protein of the complement cascade, interacts with the first and second EGF-like domains of CD97. N-glycosylation of CD97 within the EGF domains is crucial for CD55 binding.

Transgenic expression of a CD97 in mice enhanced levels of nonphosphorylated membrane-bound β-catenin and phosphorylated Akt. Furthermore, ectopic CD97 expression facilitated RhoA activation through binding of Gα12/13 as well as induced Ki67 expression and phosphorylated ERK and Akt through enhancing lysophosphatidic acid receptor 1 signaling. Lysophosphatidylethanolamine and lysophosphatidic acid use heterodimeric LPAR1–CD97 to drive Gi/o protein–phospholipase C–inositol 1,4,5-trisphosphate signaling and induce in breast cancer cells. In the immune system, CD97 is known as a critical mediator of host defense. Upon lymphoid, myeloid cells and neutrophil activation, CD97 is upregulated to promote adhesion and migration to sites of inflammation. Moreover, it has been shown. Mice lacking CD97 or its ligand CD55 have twice as many granulocytes as wild-type mice due to enhanced granulopoiesis. Antibodies against CD97 have been demonstrated to diminish various inflammatory disorders by depleting granulocytes.

Notably, CD97 antibody-mediated granulocytopenia only happens under the condition of pro-inflammation via an Fc receptor-associated mechanism. The interaction between CD97 and its ligand CD55 regulates T-cell activation and increases proliferation and cytokine production. Changes in the expression of CD97 have been described for auto-inflammatory diseases, such as rheumatoid arthritis and multiple sclerosis; the expression of CD97 on macrophage and the abundant presence of its ligand CD55 on fibroblast-like synovial cells suggest that the CD97-CD55 interaction is involved in the recruitment and/or retention of macrophages into the synovial tissue in rheumatoid arthritis. CD97 antibodies and lack of CD97 or CD55 in mice reduced synovial inflammation and joint damage in collagen- and K/BxN serum transfer-induced arthritis. In brain tissue, CD97 is undetectable in normal white matter, expression of CD55 is restricted to the endothelium. In pre-active lesion, increased expression of CD55 in endothelial cells and robust CD97 expression on infiltrating leukocytes suggest a possible role of both molecules in immune cell migration through the blood-brain barrier.

Additionally, soluble N-terminal fragment s of CD97 are detectable in the serum of patients with rheumatoid arthritis and multiple sclerosis. Outside the immune system, CD97 is involved in cell–cell interactions. CD97 in colonic enterocytes strengthens E-cadherin-based adherens junctions to maintain lateral cell-cell contacts and regulates the localization and degradation of β-catenin through glycogen synthase kinase-3β and Akt signaling. Ectopic CD97 expression upregulates the expression of N-cadherin and β-catenin in HT1080 fibrosarcoma cells leading to enhanced cell-cell aggregation. CD97 is expressed at the peripheral sarcolemma in skeletal muscle. However, lack of CD97 only affects the structure of the sarcoplasmic reticulum, but not the function of skeletal muscle. In addition, CD97 promotes angiogenesis of the endothelium through to α5β1 and αvβ3 integrins, which contributes to cell attachment. CD97 expression in cancer was first reported for dedifferentiated thyroid carcinoma and their lymph node metastases.

CD97 is expressed on many types of tumors including thyroid, pancreatic, esophageal and oral squamous carcinomas as well as glioblastoma and glioblastoma-initiating cells. In addition, enhanced CD97 expression has been found at the invasion front of tumors, suggesting a possible role in tumor migration/invasion, correlated with a poorer clinical prognosis. CD97 has isoform-specific functions in some tumors. For instance, the small EGF isoform promoted tumor invasion and metastasis in gastric carcinoma. Forced CD97 expression induced cell migration, activated proteolytic matrix metalloproteinases, enhanced secretion of the chemokines interleukin -8. Tumor suppressor microRNA-126 downregulated in cancer, was found to target CD97 thereby modulating cancer progression. CD97 can heterodimerize with the LPAR1, a canonical GPCR, implied in tumor progression, to modulate synergistic functions and LPA-mediated Rho signaling, it has been shown that CD97 regulates degradation of β-catenin. GSK-3β, inhibited in some cancer, regulates the stability of β-catenin in cytoplasm and subsequently, cytosolic β-catenin moves into the nucleus to facili