Georgia Groome

Georgia Groome

Georgia Groome is an English actress. She is best known for her roles in London to Brighton (2006) and Angus, Thongs and Perfect Snogging (2008).

arly life and education

Groome was born on 11 February 1992[1] in Nottingham,[2] the daughter of Paul Groome, a publican and chef who died in 2009, and Fiona (née Tulloch), a drama and vocal coach.

She resided in Chellaston near Shelton Lock, Derbyshire.[citation needed] Groome, at the age of nine, auditioned for a role in the touring stage version of the musical Annie Get Your Gun and got the part

She trained at Nottingham Television Workshop, Derby Youth Theatre. and Trent College.[3]

Career

After her acting debut in the TV film, A Fish Out of Water in 2001, Groome appeared in an episode of the short-lived TV series, Dangerville, playing an orphan.

When Groome was just 14 years old, she landed her first feature film role in the well-received British independent film London to Brighton in 2006, playing an 11-year-old runaway.[4] That year she was also one of the eight young adventurers on Serious Amazon for CBBC.[5] In 2007 Groome had a role in Elaine Wickham's short, My Mother.

In 2008, Groome had a minor role in comedy, horror The Cottage. Her breakthrough role was as 14-year-old, boyfriend-searching Georgia Nicolson alongside Aaron Johnson in the 2008 film Angus, Thongs and Perfect Snogging, for which she won the award for Best Child Actor at the Buster International Children's Film Festival.[1] She also had a minor role in horror film The Disappeared.

In 2009, she made her stage debut in Tusk Tusk, a new play by Polly Stenham at the Royal Court Theatre in London.[1][6] The same year, she appeared in the short Leaving Eva and an episode of The Bill. In 2010, Groome appeared in an episode of British television detective drama Lewis, as well as the short Silent Things.

In 2011, Groome starred in two shorts, The True Meaning of Love[7] and Six Degrees. She also appeared in Susan Jacobson's The Holding[8] and had a lead role in The Great Ghost Rescue, a film adaptation of Eva Ibbotson's book of the same name.[9]

She appeared alongside Stephen Dillane in Papadopoulos & Sons, in which she played snobby fashion victim Katie. The film was released in the UK through Cineworld on 5 April 2013.

Personal life

Groome has been in a relationship with Rupert Grint since 2011.[10] On April 10, 2020, it was announced that Grint and Groome were expecting their first child.

Ebola

Ebola

Ebola virus disease (EVD), or simply Ebola, is a viral haemorrhagic fever of humans and other primates caused by ebolaviruses.[1] Signs and symptoms typically start between two days and three weeks after contracting the virus with a fever, sore throat, muscular pain, and headaches.[1] Vomiting, diarrhoea and rash usually follow, along with decreased function of the liver and kidneys.[1] At this time, some people begin to bleed both internally and externally.[1] The disease has a high risk of death, killing 25% to 90% of those infected, with an average of about 50%.[1] This is often due to low blood pressure from fluid loss, and typically follows six to 16 days after symptoms appear.[2]

The virus spreads through direct contact with body fluids, such as blood from infected humans or other animals.[1] Spread may also occur from contact with items recently contaminated with bodily fluids.[1] Spread of the disease through the air between primates, including humans, has not been documented in either laboratory or natural conditions.[3] Semen or breast milk of a person after recovery from EVD may carry the virus for several weeks to months.[1][4][5] Fruit bats are believed to be the normal carrier in nature, able to spread the virus without being affected by it.[1] Other diseases such as malaria, cholera, typhoid fever, meningitis and other viral haemorrhagic fevers may resemble EVD.[1] Blood samples are tested for viral RNA, viral antibodies or for the virus itself to confirm the diagnosis.[1][6]

Control of outbreaks requires coordinated medical services and community engagement.[1] This includes rapid detection, contact tracing of those who have been exposed, quick access to laboratory services, care for those infected, and proper disposal of the dead through cremation or burial.[1][7] Samples of body fluids and tissues from people with the disease should be handled with special caution.[1] Prevention includes limiting the spread of disease from infected animals to humans by handling potentially infected bushmeat only while wearing protective clothing, and by thoroughly cooking bushmeat before eating it.[1] It also includes wearing proper protective clothing and washing hands when around a person with the disease.[1] An Ebola vaccine was approved in the United States in December 2019.[8] While there is no approved treatment for Ebola as of 2019,[9] two treatments (REGN-EB3 and mAb114) are associated with improved outcomes.[10] Supportive efforts also improve outcomes.[1] This includes either oral rehydration therapy (drinking slightly sweetened and salty water) or giving intravenous fluids as well as treating symptoms.[1]

The disease was first identified in 1976, in two simultaneous outbreaks: one in Nzara (a town in South Sudan) and the other in Yambuku (Democratic Republic of the Congo), a village near the Ebola River from which the disease takes its name.[1] EVD outbreaks occur intermittently in tropical regions of sub-Saharan Africa.[1] Between 1976 and 2013, the World Health Organization reports 24 outbreaks involving 2,387 cases with 1,590 deaths.[1][11] The largest outbreak to date was the epidemic in West Africa, which occurred from December 2013 to January 2016, with 28,646 cases and 11,323 deaths.[12][13][14] It was declared no longer an emergency on 29 March 2016.[15] Other outbreaks in Africa began in the Democratic Republic of the Congo in May 2017,[16][17] and 2018.[18][19] In July 2019, the World Health Organization declared the Congo Ebola outbreak a world health emergency.[20]

Onset

The length of time between exposure to the virus and the development of symptoms (incubation period) is between two and 21 days,[1][21] and usually between four and ten days.[22] However, recent estimates based on mathematical models predict that around 5% of cases may take greater than 21 days to develop.[23]

Symptoms usually begin with a sudden influenza-like stage characterised by feeling tired, fever, weakness, decreased appetite, muscular pain, joint pain, headache, and sore throat.[1][22][24][25] The fever is usually higher than 38.3 °C (101 °F).[26] This is often followed by nausea, vomiting, diarrhoea, abdominal pain, and sometimes hiccups.[25][27] The combination of severe vomiting and diarrhoea often leads to severe dehydration.[28] Next, shortness of breath and chest pain may occur, along with swelling, headaches, and confusion.[25] In about half of the cases, the skin may develop a maculopapular rash, a flat red area covered with small bumps, five to seven days after symptoms begin.[22][26]

Bleeding

In some cases, internal and external bleeding may occur.[1] This typically begins five to seven days after the first symptoms.[29] All infected people show some decreased blood clotting.[26] Bleeding from mucous membranes or from sites of needle punctures has been reported in 40–50% of cases.[30] This may cause vomiting blood, coughing up of blood, or blood in stool.[31] Bleeding into the skin may create petechiae, purpura, ecchymoses or haematomas (especially around needle injection sites).[32] Bleeding into the whites of the eyes may also occur.[33] Heavy bleeding is uncommon; if it occurs, it is usually in the gastrointestinal tract.[34] The incidence of bleeding into the gastrointestinal tract was reported to be ~58% in the 2001 outbreak in Gabon,[35] but in the 2014-15 outbreak in the US it was ~18%,[36] possibly due to improved prevention of disseminated intravascular coagulation.[28]

Recovery and death

Recovery may begin between seven and 14 days after first symptoms.[25] Death, if it occurs, follows typically six to sixteen days from first symptoms and is often due to low blood pressure from fluid loss.[2] In general, bleeding often indicates a worse outcome, and blood loss may result in death.[24] People are often in a coma near the end of life.[25]

Those who survive often have ongoing muscular and joint pain, liver inflammation, and decreased hearing, and may have continued tiredness, continued weakness, decreased appetite, and difficulty returning to pre-illness weight.[25][37] Problems with vision may develop.[38]

Survivors develop antibodies against Ebola that last at least 10 years, but it is unclear whether they are immune to additional infections.[39]

Cause

EVD in humans is caused by four of five viruses of the genus Ebolavirus. The four are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV) and one simply called Ebola virus (EBOV, formerly Zaire Ebola virus).[40] EBOV, species Zaire ebolavirus, is the most dangerous of the known EVD-causing viruses, and is responsible for the largest number of outbreaks.[41] The fifth virus, Reston virus (RESTV), is not thought to cause disease in humans, but has caused disease in other primates.[42][43] All five viruses are closely related to marburgviruses.[40]

Virology

Ebolaviruses contain single-stranded, non-infectious RNA genomes.[44] Ebolavirus genomes contain seven genes including 3'-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5'-UTR.[32][45] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV and TAFV) differ in sequence and the number and location of gene overlaps. As with all filoviruses, ebolavirus virions are filamentous particles that may appear in the shape of a shepherd's crook, of a "U" or of a "6," and they may be coiled, toroid or branched.[45][46] In general, ebolavirions are 80 nanometers (nm) in width and may be as long as 14,000 nm.[47]

Their life cycle is thought to begin with a virion attaching to specific cell-surface receptors such as C-type lectins, DC-SIGN, or integrins, which is followed by fusion of the viral envelope with cellular membranes.[48] The virions taken up by the cell then travel to acidic endosomes and lysosomes where the viral envelope glycoprotein GP is cleaved.[48] This processing appears to allow the virus to bind to cellular proteins enabling it to fuse with internal cellular membranes and release the viral nucleocapsid.[48] The Ebolavirus structural glycoprotein (known as GP1,2) is responsible for the virus' ability to bind to and infect targeted cells.[49] The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. The most abundant protein produced is the nucleoprotein, whose concentration in the host cell determines when L switches from gene transcription to genome replication. Replication of the viral genome results in full-length, positive-strand antigenomes that are, in turn, transcribed into genome copies of negative-strand virus progeny.[50] Newly synthesised structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane from which they bud. The mature progeny particles then infect other cells to repeat the cycle. The genetics of the Ebola virus are difficult to study because of EBOV's virulent characteristics.[51]

Transmission

It is believed that between people, Ebola disease spreads only by direct contact with the blood or other body fluids of a person who has developed symptoms of the disease.[52][53][54] Body fluids that may contain Ebola viruses include saliva, mucus, vomit, feces, sweat, tears, breast milk, urine and semen.[4][39] The WHO states that only people who are very sick are able to spread Ebola disease in saliva, and whole virus has not been reported to be transmitted through sweat. Most people spread the virus through blood, feces and vomit.[55] Entry points for the virus include the nose, mouth, eyes, open wounds, cuts and abrasions.[39] Ebola may be spread through large droplets; however, this is believed to occur only when a person is very sick.[56] This contamination can happen if a person is splashed with droplets.[56] Contact with surfaces or objects contaminated by the virus, particularly needles and syringes, may also transmit the infection.[57][58] The virus is able to survive on objects for a few hours in a dried state, and can survive for a few days within body fluids outside of a person.[39][59]

The Ebola virus may be able to persist for more than three months in the semen after recovery, which could lead to infections via sexual intercourse.[4][60][61] Virus persistence in semen for over a year has been recorded in a national screening programme.[62] Ebola may also occur in the breast milk of women after recovery, and it is not known when it is safe to breastfeed again.[5] The virus was also found in the eye of one patient in 2014, two months after it was cleared from his blood.[63] Otherwise, people who have recovered are not infectious.[57]

The potential for widespread infections in countries with medical systems capable of observing correct medical isolation procedures is considered low.[64] Usually when someone has symptoms of the disease, they are unable to travel without assistance.[65]

Dead bodies remain infectious; thus, people handling human remains in practices such as traditional burial rituals or more modern processes such as embalming are at risk.[64] 69% of the cases of Ebola infections in Guinea during the 2014 outbreak are believed to have been contracted via unprotected (or unsuitably protected) contact with infected corpses during certain Guinean burial rituals.[66][67]

Health-care workers treating people with Ebola are at greatest risk of infection.[57] The risk increases when they do not have appropriate protective clothing such as masks, gowns, gloves and eye protection; do not wear it properly; or handle contaminated clothing incorrectly.[57] This risk is particularly common in parts of Africa where the disease mostly occurs and health systems function poorly.[68] There has been transmission in hospitals in some African countries that reuse hypodermic needles.[69][70] Some health-care centres caring for people with the disease do not have running water.[71] In the United States the spread to two medical workers treating infected patients prompted criticism of inadequate training and procedures.[72]

Human-to-human transmission of EBOV through the air has not been reported to occur during EVD outbreaks,[3] and airborne transmission has only been demonstrated in very strict laboratory conditions, and then only from pigs to primates, but not from primates to primates.[52][58] Spread of EBOV by water, or food other than bushmeat, has not been observed.[57][58] No spread by mosquitos or other insects has been reported.[57] Other possible methods of transmission are being studied.[59]

Airborne transmission among humans is theoretically possible due to the presence of Ebola virus particles in saliva, which can be discharged into the air with a cough or sneeze, but observational data from previous epidemics suggests the actual risk of airborne transmission is low.[73] A number of studies examining airborne transmission broadly concluded that transmission from pigs to primates could happen without direct contact because, unlike humans and primates, pigs with EVD get very high ebolavirus concentrations in their lungs, and not their bloodstream.[74] Therefore, pigs with EVD can spread the disease through droplets in the air or on the ground when they sneeze or cough.[75] By contrast, humans and other primates accumulate the virus throughout their body and specifically in their blood, but not very much in their lungs.[75] It is believed that this is the reason researchers have observed pig to primate transmission without physical contact, but no evidence has been found of primates being infected without actual contact, even in experiments where infected and uninfected primates shared the same air.[74][75]

Initial case

Although it is not entirely clear how Ebola initially spreads from animals to humans, the spread is believed to involve direct contact with an infected wild animal or fruit bat.[57] Besides bats, other wild animals sometimes infected with EBOV include several monkey species, chimpanzees, gorillas, baboons, and duikers.[79]

Animals may become infected when they eat fruit partially eaten by bats carrying the virus.[80] Fruit production, animal behavior and other factors may trigger outbreaks among animal populations.[80]

Evidence indicates that both domestic dogs and pigs can also be infected with EBOV.[81] Dogs do not appear to develop symptoms when they carry the virus, and pigs appear to be able to transmit the virus to at least some primates.[81] Although some dogs in an area in which a human outbreak occurred had antibodies to EBOV, it is unclear whether they played a role in spreading the disease to people.[81]

Reservoir

The natural reservoir for Ebola has yet to be confirmed; however, bats are considered to be the most likely candidate species.[58] Three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata) were found to possibly carry the virus without getting sick.[82] As of 2013, whether other animals are involved in its spread is not known.[81] Plants, arthropods, rodents, and birds have also been considered possible viral reservoirs.[1][28]

Bats were known to roost in the cotton factory in which the first cases of the 1976 and 1979 outbreaks were observed, and they have also been implicated in Marburg virus infections in 1975 and 1980.[83] Of 24 plant and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected.[84] The bats displayed no clinical signs of disease, which is considered evidence that these bats are a reservoir species of EBOV. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA.[85] Antibodies against Zaire and Reston viruses have been found in fruit bats in Bangladesh, suggesting that these bats are also potential hosts of the virus and that the filoviruses are present in Asia.[86]

Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians and arthropods sampled from regions of EBOV outbreaks, no Ebola virus was detected apart from some genetic traces found in six rodents (belonging to the species Mus setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic.[83][87] However, further research efforts have not confirmed rodents as a reservoir.[88] Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high rates of death in these species resulting from EBOV infection make it unlikely that these species represent a natural reservoir for the virus.[83]

Deforestation has been mentioned as a possible contributor to recent outbreaks, including the West African Ebola virus epidemic. Index cases of EVD have often been close to recently deforested lands.[89][90]

Pathophysiology

Like other filoviruses, EBOV replicates very efficiently in many cells, producing large amounts of virus in monocytes, macrophages, dendritic cells and other cells including liver cells, fibroblasts, and adrenal gland cells.[91] Viral replication triggers high levels of inflammatory chemical signals and leads to a septic state.[37]

EBOV is thought to infect humans through contact with mucous membranes or skin breaks.[52] After infection, endothelial cells (cells lining the inside of blood vessels), liver cells, and several types of immune cells such as macrophages, monocytes, and dendritic cells are the main targets of attack.[52] Following infection, immune cells carry the virus to nearby lymph nodes where further reproduction of the virus takes place.[52] From there the virus can enter the bloodstream and lymphatic system and spread throughout the body.[52] Macrophages are the first cells infected with the virus, and this infection results in programmed cell death.[47] Other types of white blood cells, such as lymphocytes, also undergo programmed cell death leading to an abnormally low concentration of lymphocytes in the blood.[52] This contributes to the weakened immune response seen in those infected with EBOV.[52]

Endothelial cells may be infected within three days after exposure to the virus.[47] The breakdown of endothelial cells leading to blood vessel injury can be attributed to EBOV glycoproteins. This damage occurs due to the synthesis of Ebola virus glycoprotein (GP), which reduces the availability of specific integrins responsible for cell adhesion to the intercellular structure and causes liver damage, leading to improper clotting. The widespread bleeding that occurs in affected people causes swelling and shock due to loss of blood volume.[92] The dysfunctional bleeding and clotting commonly seen in EVD has been attributed to increased activation of the extrinsic pathway of the coagulation cascade due to excessive tissue factor production by macrophages and monocytes.[22]

After infection, a secreted glycoprotein, small soluble glycoprotein (sGP or GP) is synthesised. EBOV replication overwhelms protein synthesis of infected cells and the host immune defences. The GP forms a trimeric complex, which tethers the virus to the endothelial cells. The sGP forms a dimeric protein that interferes with the signalling of neutrophils, another type of white blood cell. This enables the virus to evade the immune system by inhibiting early steps of neutrophil activation.[medical citation needed]

Immune system evasion

Filoviral infection also interferes with proper functioning of the innate immune system.[48][50] EBOV proteins blunt the human immune system's response to viral infections by interfering with the cells' ability to produce and respond to interferon proteins such as interferon-alpha, interferon-beta, and interferon gamma.[49][93]

The VP24 and VP35 structural proteins of EBOV play a key role in this interference. When a cell is infected with EBOV, receptors located in the cell's cytosol (such as RIG-I and MDA5) or outside of the cytosol (such as Toll-like receptor 3 (TLR3), TLR7, TLR8 and TLR9) recognise infectious molecules associated with the virus.[49] On TLR activation, proteins including interferon regulatory factor 3 and interferon regulatory factor 7 trigger a signalling cascade that leads to the expression of type 1 interferons.[49] The type 1 interferons are then released and bind to the IFNAR1 and IFNAR2 receptors expressed on the surface of a neighbouring cell.[49] Once interferon has bound to its receptors on the neighbouring cell, the signalling proteins STAT1 and STAT2 are activated and move to the cell's nucleus.[49] This triggers the expression of interferon-stimulated genes, which code for proteins with antiviral properties.[49] EBOV's V24 protein blocks the production of these antiviral proteins by preventing the STAT1 signalling protein in the neighbouring cell from entering the nucleus.[49] The VP35 protein directly inhibits the production of interferon-beta.[93] By inhibiting these immune responses, EBOV may quickly spread throughout the body.[47]

Diagnosis

When EVD is suspected, travel, work history, and exposure to wildlife are important factors with respect to further diagnostic efforts.[medical citation needed]

Laboratory testing

Possible non-specific laboratory indicators of EVD include a low platelet count; an initially decreased white blood cell count followed by an increased white blood cell count; elevated levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST); and abnormalities in blood clotting often consistent with disseminated intravascular coagulation (DIC) such as a prolonged prothrombin time, partial thromboplastin time, and bleeding time.[94] Filovirions such as EBOV may be identified by their unique filamentous shapes in cell cultures examined with electron microscopy.[95]

The specific diagnosis of EVD is confirmed by isolating the virus, detecting its RNA or proteins, or detecting antibodies against the virus in a person's blood.[96] Isolating the virus by cell culture, detecting the viral RNA by polymerase chain reaction (PCR)[6][22] and detecting proteins by enzyme-linked immunosorbent assay (ELISA) are methods best used in the early stages of the disease and also for detecting the virus in human remains.[6][96] Detecting antibodies against the virus is most reliable in the later stages of the disease and in those who recover.[96] IgM antibodies are detectable two days after symptom onset and IgG antibodies can be detected six to 18 days after symptom onset.[22] During an outbreak, isolation of the virus with cell culture methods is often not feasible. In field or mobile hospitals, the most common and sensitive diagnostic methods are real-time PCR and ELISA.[97] In 2014, with new mobile testing facilities deployed in parts of Liberia, test results were obtained 3–5 hours after sample submission.[98] In 2015, a rapid antigen test which gives results in 15 minutes was approved for use by WHO.[99] It is able to confirm Ebola in 92% of those affected and rule it out in 85% of those not affected.[99]

Differential diagnosis

Early symptoms of EVD may be similar to those of other diseases common in Africa, including malaria and dengue fever.[24] The symptoms are also similar to those of other viral haemorrhagic fevers such as Marburg virus disease, Crimean Congo haemorrhagic fever, and Lassa fever.[100][101]

The complete differential diagnosis is extensive and requires consideration of many other infectious diseases such as typhoid fever, shigellosis, rickettsial diseases, cholera, sepsis, borreliosis, EHEC enteritis, leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, measles, and viral hepatitis among others.[102]

Non-infectious diseases that may result in symptoms similar to those of EVD include acute promyelocytic leukaemia, haemolytic uraemic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary haemorrhagic telangiectasia, Kawasaki disease, and warfarin poisoning

Kimberley Walsh

Kimberley Walsh

Kimberley Jane Scott[2] (née Walsh; born 20 November 1981)[1] is an English singer, model, television presenter, actress and dancer. She rose to fame in late 2002 when she auditioned for the reality series Popstars: The Rivals on ITV. The series announced that Walsh had won a place as a member of the girl group Girls Aloud.[3] The group achieved large success, having twenty consecutive top ten singles (including four number ones) in the UK, six studio albums have all been certified platinum by the British Phonographic Industry (BPI), two of which went to number one in the UK, and accumulating a total of five BRIT Award nominations. In 2009, Girls Aloud won "Best Single" with their song "The Promise".

During the group's hiatus, Walsh embarked on acting and presenting. In July 2010, she became a presenter on the music talkshow, Suck My Pop and presented coverage for the BAFTA Awards. In 2011, she appeared in Horrid Henry: The Movie as Prissy Polly. Musically, Walsh has featured on Aggro Santos's "Like U Like". In 2012, Walsh made her West End theatre debut, playing Princess Fiona in the London production of Shrek the Musical. She also fronted the 2009 Autumn/Winter collection for the fashion chain New Look and, in January 2011, she was revealed as the new face of Puma AG. In 2012, Walsh took part in Strictly Come Dancing, where she finished as one of the runners-up.

Since 2011, after making her West End debut in Shrek, Walsh has returned to perform in stage versions popular films such as Elf in 2015, before Big and Sleepless in Seattle both in 2019.

Early life

Walsh was born in Bradford, West Yorkshire,[1][4] the daughter of John and Diane Walsh. She grew up with three siblings, Sally Walsh, Amy Walsh and Adam Walsh in Allerton, West Yorkshire.[1] Sally played the character of Lyn Hutchinson on the soap opera Emmerdale between 1997 and 2000,[1] and Amy joined the show's cast in 2014 as Tracy Shankley.[5]

Walsh attended Sandy Lane Primary School, Stoney Lee Middle School, and Beckfoot Grammar School,[6] and had her first taste of fame appearing in an advert as a child along with sister Sally in an Asda advert. She starred as Young Cosette in a regional production of Les Misérables and starred in ITV's The Book Tower in 1986.[citation needed] Walsh attended the Bradford theatre school, Stage 84, and briefly taught there.

Music career

Girls Aloud

Walsh auditioned for the reality television show Popstars The Rivals in 2002 with the song "Where Do Broken Hearts Go".[7] Several thousand applicants attended auditions across the UK in hope of being selected. Ten girls and ten boys were chosen as finalists by judges Pete Waterman, Louis Walsh and Geri Halliwell. Walsh did not initially make it into the group of ten female contestants who were to appear on the show. However, when another contestant was disqualified on a technicality, she found herself on the show. These finalists then took to the stage participating in weekly Saturday night live performances which alternated weekly between the girls and boys. Each week, the contestant polling the fewest phone votes was eliminated, until the final line-ups of the groups emerged. Walsh joined Nadine Coyle, Sarah Harding, Nicola Roberts, and Cheryl Tweedy to comprise the new girl group Girls Aloud, formed through the show by a public vote on 30 November 2002

The group's debut single "Sound of the Underground" peaked at number one on the UK Singles Chart, becoming the 2002 Christmas number one.[8] Girls Aloud hold the record for the shortest time between formation and reaching number one.[9] The group released their debut album Sound of the Underground in May 2003,[10] which entered the charts at number two and was certified platinum by the British Phonographic Industry (BPI) later the same year. Their singles "I'll Stand by You", "Walk This Way", and "The Promise" have charted at number one. Two of their albums have reached the top of the UK Albums Chart: their greatest hits album The Sound of Girls Aloud and 2008's Out of Control, both of which entered the chart at number one, with over one million copies of the former being sold.[11]

They also achieved seven certified albums and have been nominated for five Brit Awards, winning the 2009 Best Single for "The Promise".

The group's musical style is pop, but throughout their career they had experimented with electropop and dance-pop. Girls Aloud's collaborations with Brian Higgins and his songwriting and production team Xenomania earned the group critical acclaim,[12] due to an innovative approach to mainstream pop music. The group became one of the few UK reality television acts to achieve continued success, amassing a fortune of £30 million by May 2010. Guinness World Records lists them as "Most Successful Reality TV Group" in the 2007 edition. They also hold the record for "Most Consecutive Top Ten Entries in the UK by a Female Group" in the 2008 edition, and are credited again for "Most Successful Reality TV Group" in the 2011 edition. The group was also named the United Kingdom's biggest selling girl group of the 21st century, with over 4.3 million singles sales and 4 million albums sold in the UK alone.[13][14]

In July 2009, Girls Aloud announced they would take a year-long hiatus to pursue solo projects.[15] In August 2010, bandmate Nicola Roberts revealed that she was not anticipating a reunion of Girls Aloud until 2012.[16] Walsh had revealed that she does not think it is possible Girls Aloud will ever "officially break up". She explained that they are planning to tour again and will probably take breaks from time to time, doing solo projects but they will never permanently go their separate ways.[17]

After Girls Aloud's three years of hiatus, the group reunited for their 10th anniversary. The group released their new single, "Something New" on 18 November 2012. The music video for the song was filmed in October 2012, and premiered on YouTube on 19 October 2012.[18] The song was also the official charity single for Children in Need in 2012. The group released their second greatest hits compilation, Ten on 26 November 2012. In 2013, the group embarked on Ten - The Hits Tour 2013. They announced their split soon after the tour ended.[19][20]

Solo work

It was first rumoured that Walsh was about to make a record deal with her band's record label, Fascination Records,[21] although nothing has been confirmed. Soon after the rumour, Walsh confirmed on Suck My Pop, a programme that she co-hosts on the television channel Viva in the United Kingdom, that she will feature on English rapper Aggro Santos' upcoming single, "Like U Like". The track will be her first step away from Girls Aloud as a singer. Walsh was asked for OK! Magazine: "Kimberley, there are rumours, that you will be releasing a solo album..." and Walsh said: "Gosh! I haven't got any plan to do that. Gary Barlow signed Aggro Santos and he asked me to sing Like U Like, and I've done a song for the Horrid Henry film that I'm in titled "Everybody Dance". I'm not sure about doing anything big on my own just yet." In 2012 she made her West End theatre debut, playing Princess Fiona in the London production of Shrek the Musical. The announcement came after Amanda Holden announced her pregnancy in August 2011.[22] Walsh teamed up with Alfie Boe to record a version of Queen's "One Vision" as the Official Olympic Team Great Britain Single. Walsh has also performed with several artists including Neyo with "Hate That I Love You", Ronan Keating's "No Matter What" and James Cullum with "Rainy Days and Mondays". In August 2012 it was announced that Walsh is in discussions with Gary Barlow to release a solo album for a 2013 release.

On 7 September 2012, Walsh was announced as one of the 14 celebrities, competing in tenth series of Strictly Come Dancing.[23] Her professional partner is last year's runner-up Pasha Kovalev.[24] She received 3 perfect 40s during the series, and she finished as one of the runners-up alongside presenter Denise Van Outen, behind the winner Olympian Louis Smith.

On 4 February 2013 Walsh released, through Decca Records, her debut album Centre Stage which features a series of popular musical tunes as well as two brand new tracks.[25]

Walsh has written her own autobiography, called A Whole Lot of History. The book was released on 26 September 2013.

In March 2014, Walsh took part in recording England's 2014 World Cup song. She collaborated with the likes of fellow pop stars Melanie C, Eliza Doolittle, Emma Bunton, Conor Maynard, Katy B and Pixie Lott, on "Greatest Day", a track originally performed by British band, Take That. The track was produced by Gary Barlow and recorded at Sarm Studios in London. The track also featured past footballers such as Gary Lineker, Michael Owen, Geoff Hurst, David Seaman, Peter Shilton, Glenn Hoddle and Dion Dublin on backing vocals.[26]

Television

Acting

Before Walsh became a member of Girls Aloud, she had worked in theatre and acting.[27] In 2000 Walsh appeared in the television series This Is Personal: The Hunt for the Yorkshire Ripper as Gillian Oldfield, and starred in a BBC Educational Schools programme called Focus. In the same year, Walsh applied for the role of Maria Sutherland in Coronation Street. However, she lost out to Samia Ghadie.[28] In 2001, Walsh played Tracy in Dream Back. In 2007, alongside her bandmates she appeared in St. Trinian's playing a school band member. In 2008 she and bandmate Nicola Roberts had small parts in Britannia High, in which they played themselves. Walsh has recently stated that she would like to star in a musical in the future, playing a stage role.[29] In late 2010, Walsh landed a role in the live-action 3D family comedy film Horrid Henry: The Movie as the titular character's overactive cousin Prissy Polly, with the film being released on 29 July 2011. Walsh also appeared in the 2013 movie All Stars, alongside Theo Stevenson once again, who she appeared with first in Horrid Henry: The Movie. She plays the minor role of his character's mother.

On 5 October 2011 through 21 May 2012 she made her West End theatre debut, playing Princess Fiona in the London production of Shrek the Musical. The announcement came after Amanda Holden announced her pregnancy in August 2011.[22] Originally signed on until 27 February 2012, she extended her run to 21 May 2012. She subsequently returned to the West End stage in October 2015, playing the role of Jovie in Elf: The Musical.[30]

In 2018 she was cast in series two of Ackley Bridge as the character, Claire Butterworth.

In autumn 2019, Walsh returned to the west end in the cast of BIG the Musical.

Presenting

Walsh appeared in Let's Dance for Sport Relief as a panellist and also fronted coverage of the BAFTA Awards for MTV on her own programme Kimberley Walsh at the BAFTAS in 2010 and in the summer of 2010 hosted sky 1 documentary "Girl in the Blue Jeans". She also presented coverage for The X Factor live from South Shields on the day of the final in 2009 for Joe McElderry. On 17 – 18 June 2010, Walsh hosted Channel 4's The 5 O'Clock Show with Stephen Mulhern. Walsh appeared in her own documentary for Sky 1 named Kimberley Walsh: Blue Jean Girl which aired on Wednesday, 17 June 2010. On the same day, Walsh appeared on This Morning to promote the show. Walsh later became a presenter of new music talk-show, titled Suck My Pop, on Viva. Walsh also starred as a judge for ITV's entertainment show Born To Shine.

On the 9 April 2016, Walsh co-presented Weekend Brunch the Grand National Day special with Tim Lovejoy.

Other ventures

Walsh climbed Mount Kilimanjaro in aid of Comic Relief in March 2009. The climb, organised by Gary Barlow, was also undertaken by fellow Girls Aloud member Cheryl, Alesha Dixon, Fearne Cotton, Denise Van Outen, Chris Moyles, Ben Shephard, Ronan Keating and Barlow himself. Between 3 February and 23 March 2009, Walsh, Cole, Barlow, Moyles and Cotton also raised money for Comic Relief by providing the voice for the BT Speaking Clock.[citation needed]

As of 26 August 2009, Walsh was modelling for the clothing line New Look following in the footsteps of Lily Allen and Alexa Chung.[citation needed] Walsh became OK! magazine's new weekly columnist in August 2010. The column is called "Kimberley Calls The Shots".[31]

She was also named as the new face and hair of Schwarzkopf for a reported 6 figure deal.[32] In March 2011, Walsh teamed up with Tess Daly and Joanna Page to work with Maltesers to promote Red Nose Day 2011.[33] In January 2011, Walsh was revealed as the new face of Puma AG BodyTrain fitness toner wear.[34] In May 2011, Walsh was named as the face of Right Guard's Xtreme Dry Range.[35]

In 2017, Kimberley launched a children’s clothing line called “Kimba’s Kids” which she runs with her brother. In September 2019, she signed with outdoor clothing company Regatta.

Krakatoa

Krakatoa

Krakatoa, or Krakatau (Indonesian: Krakatau), is a caldera[2] in the Sunda Strait between the islands of Java and Sumatra in the Indonesian province of Lampung. The caldera is part of a volcanic island group (Krakatoa Archipelago) comprising four islands: two of which, Lang and Verlaten, are remnants of a previous volcanic edifice destroyed in eruptions long before the famous 1883 eruption; another, Rakata, is the remnant of a much larger island destroyed in the 1883 eruption.

In 1927, a fourth island, Anak Krakatau, or "Child of Krakatoa", emerged from the caldera formed in 1883. There has been new eruptive activity since the late 20th century, with a large collapse causing a deadly tsunami in December 2018.

The most notable eruptions of Krakatoa culminated in a series of massive explosions over 26–27 August 1883, which were among the most violent volcanic events in recorded history.

With an estimated Volcanic Explosivity Index (VEI) of 6,[3] the eruption was equivalent to 200 megatons of TNT (840 PJ)—about 13,000 times the nuclear yield of the Little Boy bomb (13 to 16 kt) that devastated Hiroshima, Japan, during World War II, and four times the yield of Tsar Bomba, the most powerful nuclear device ever detonated at 50 Mt.

The 1883 eruption ejected approximately 25 km3 (6 cubic miles) of rock.[4] The cataclysmic explosion was heard 3,600 km (2,200 mi) away in Alice Springs, Australia, and on the island of Rodrigues near Mauritius, 4,780 km (2,970 mi) to the west.[5]

According to the official records of the Dutch East Indies colony, 165 villages and towns were destroyed near Krakatoa, and 132 were seriously damaged. At least 36,417 people died, and many more thousands were injured, mostly from the tsunamis that followed the explosion. The eruption destroyed two-thirds of the island of Krakatoa.

Eruptions in the area since 1927 have built a new island at the same location, named Anak Krakatau (which is Indonesian for "Child of Krakatoa"). Periodic eruptions have continued since, with recent eruptions in 2009, 2010, 2011, and 2012, and a major collapse in 2018. In late 2011, this island had a radius of roughly 2 kilometres (1.2 mi), and a highest point of about 324 metres (1,063 ft) above sea level,[6] growing five metres (16 ft) each year.[7] In 2017, the height of Anak Krakatau was reported as over 400 m (1,300 ft) above sea level;[8] following a collapse in December 2018, the height was reduced to 110 meters (361 ft).[9][6]

Etymology

Although there are earlier descriptions of an island in the Sunda Strait with a "pointed mountain," the earliest mention of Krakatoa by name in the western world was on a 1611 map by Lucas Janszoon Waghenaer, who labelled the island "Pulo Carcata" (pulo is the Sundanese word for "island"). About two dozen variants have been found, including Crackatouw, Cracatoa, and Krakatao (in an older Portuguese-based spelling). The first known appearance of the spelling Krakatau was by Wouter Schouten, who passed by "the high tree-covered island of Krakatau" in October 1658.[10]

The origin of the Indonesian name Krakatau is uncertain.[11]

The Smithsonian Institution's Global Volcanism Program cites the Indonesian name, Krakatau, as the correct name, but says that Krakatoa is often employed.[7][12][13]

Geographical setting

Indonesia has over 130 active volcanoes,[14] the most of any nation. They make up the axis of the Indonesian island arc system produced by northeastward subduction of the Indo-Australian Plate. A majority of these volcanoes lie along Indonesia's two largest islands, Java and Sumatra. These two islands are separated by the Sunda Strait located at a bend in the axis of the island arc. Krakatau is directly above the subduction zone of the Eurasian Plate and the Indo-Australian Plate where the plate boundaries make a sharp change of direction, possibly resulting in an unusually weak crust in the region.

Pre-1883 history

At some point in prehistory, an earlier caldera-forming eruption had occurred, leaving as remnants Verlaten (or Sertung); Lang (also known as Rakata Kecil, or Panjang); Poolsche Hoed ("Polish Hat");[15] and the base of Rakata. Later, at least two more cones (Perboewatan and Danan) formed and eventually joined with Rakata, forming the main island of Krakatoa.[16] At the time of the 1883 eruption, the Krakatoa group comprised Lang, Verlaten, and Krakatoa itself, an island 9 km (5.6 mi) long by 5 km (3.1 mi) wide. There were also the tree-covered islet near Lang (Poolsche Hoed) and several small rocky islets or banks between Krakatoa and Verlaten.

There were three volcanic cones on Krakatoa island: Rakata, (820 m or 2,690 ft) to the south; Danan, (450 m or 1,480 ft) near the center; and Perboewatan, (120 m or 390 ft) to the north.

416 AD event

The Javanese Book of Kings (Pustaka Raja) records that in the year 338 Saka (416 AD):

A thundering sound was heard from the mountain Batuwara [now called Pulosari, an extinct volcano in Bantam, the nearest to the Sunda Strait] which was answered by a similar noise from Kapi, lying westward of the modern Bantam [(Banten) is the westernmost province in Java, so this seems to indicate that Krakatoa is meant]. A great glowing fire, which reached the sky, came out of the last-named mountain; the whole world was greatly shaken and violent thundering, accompanied by heavy rain and storms took place, but not only did not this heavy rain extinguish the eruption of the fire of the mountain Kapi, but augmented the fire; the noise was fearful, at last the mountain Kapi with a tremendous roar burst into pieces and sank into the deepest of the earth. The water of the sea rose and inundated the land, the country to the east of the mountain Batuwara, to the mountain Rajabasa [the most southerly volcano in Sumatra], was inundated by the sea; the inhabitants of the northern part of the Sunda country to the mountain Rajabasa were drowned and swept away with all property[17] ... The water subsided but the land on which Kapi stood became sea, and Java and Sumatra were divided into two parts.

There is no geological evidence of a Krakatoa eruption of this size around that time; it may describe loss of land which previously joined Java to Sumatra across what is now the narrow east end of the Sunda Strait; or it may be a mistaken date, referring to a later eruption in 535 AD, for which there is some corroborating historical evidence.[18]

535 AD event

David Keys, Ken Wohletz, and others have postulated that a violent volcanic eruption, possibly of Krakatoa, in 535 may have been responsible for the global climate changes of 535–536.[18] Keys explores what he believes to be the radical and far-ranging global effects of just such a putative 6th-century eruption in his book Catastrophe: An Investigation into the Origins of the Modern World. This eruption was believed to have been even more violent than Krakatoa's 1883 eruption, and also the one that created Krakatoa's original caldera, which resulted in the creation of Verlaten Island and Lang Island.[19] However, there are other explanations for the climate change, including an eruption of Ilopango in El Salvador, in Central America.

Thornton mentions that Krakatoa was known as "The Fire Mountain" during Java's Sailendra dynasty, with records of seven eruptive events between the 9th and 16th centuries.[20] These have been tentatively dated as having occurred in 850, 950, 1050, 1150, 1320, and 1530.

1680

In February 1681, Johann Wilhelm Vogel, a Dutch mining engineer at Salida, Sumatra (near Padang), on his way to Batavia (now Jakarta) passed through the Sunda Strait. In his diary he wrote:

...I saw with amazement that the island of Krakatoa, on my first trip to Sumatra [June 1679] completely green and healthy with trees, lay completely burnt and barren in front of our eyes and that at four locations was throwing up large chunks of fire. And when I asked the ship's Captain when the aforementioned island had erupted, he told me that this had happened in May 1680 ... He showed me a piece of pumice as big as his fist.

Vogel spent several months in Batavia, returning to Sumatra in November 1681. On the same ship were several other Dutch travellers, including Elias Hesse, a writer. Hesse's journal reports:

...on the 19th [of November 1681] we again lifted anchor and proceeded first to the north of us to the island of Sleepzie (Sebesi), uninhabited, ... and then still north of the island of Krakatou, which erupted about a year ago and also is uninhabited. The rising smoke column of this island can be seen from miles away; we were with our ship very close to shore and we could see the trees sticking out high on the mountain, and which looked completely burned, but we could not see the fire itself.[21]

The eruption was also reported by a Bengali sea captain, who wrote of the event later, but had not recorded it at the time in the ship's log.[22] Neither Vogel nor Hesse mention Krakatoa in any real detail in their other passages, and no other travellers at the time mention an eruption or evidence of one. (In November 1681, a pepper crop was being offered for sale by inhabitants.)[23] In 1880, Verbeek investigated a fresh unweathered lava flow at the northern coast of Perboewatan, which could not have been more than two centuries old.

انفلونزا الطيور

انفلونزا الطيور

إنفلونزا الطيور أو خُنان الطيور[محل شك]هو مرض طيور معدي سببه فيروسات الإنفلونزا أي (Influenza A viruses). الطيور المائية المهاجرة - بشكل خاص البطّ البري - تشكل مستودعا طبيعيا لكلّ فيروسات الإنفلونزا أ

أنفلونزا الطيور هو مرض يسببه نوع من أنواع فيروس الأنفلونزا تطور وتكيف في أجسام الطيور. النوع الأخطر من هذا الفيروس هو أنفلونزا الطيور شديدة الإمراض (HPAI).

مصطلح "أنفلونزا الطيور" مشابه لأنفلونزا الكلاب أو الأحصنة أو الخنازير في أنه يشير إلى مرض تسببه سلالة من فيروسات الأنفلونزا تطورت وتكيفت في جسم مضيف معين. من الأنواع الثلاثة لفيروس الأنفلونزا A, B, وC, فيروس A هو فيروس حيواني المنشأ يمكنه الانتقال إلى الإنسان حيث أكبر مستودع طبيعي لهذه الفيروسات في الطيور. في معظم الأحيان, يشير أنفلونزا الطيور إلى فيروسات الأنفلونزا من النوع A.

بالرغم من أن فيروس أنفلونزا الطيور (أنفلونزا A) يتطور داخل أجسام الطيور, يستطيع الفيروس أن يتطور داخل جسم الإنسان وينتقل من إنسان إلى آخر. أبحاث مؤخرة في جينات الأنفلونزا الإسبانية أظهرت بأن هذا الفيروس تكيف في أجسام الإنسان والطيور. الخنازير معرضة للإصابة بفيروسات أنفلونزا البشر, الخنازير, والطيور, مما قد يسمح بإعادة تشكيل جينات الفيروسات, منتجة صنف فرعي جديد من فيروس أنفلونزا A ليس للبشر مناعة كافية لمقاومته.

يقسم أنفلونزا الطيور إلى قسمين بناء على الإمراض: شديدة الإمراض (HPAI), وضعيفة الإمراض (LPAI). الصنف المعروف بشكل أوسع من فيروسات أنفلونزا الطيور الممرضة للغاية, H5N1, ظهر في الصين عام 1996, وقد ظهر بشكل ضعيف الإمراض أيضا في أمريكا الشمالية. من غير المرجح أن تصاب الطيور الأليفة في الأقفاص بأنفلونزا الطيور, حيث لم ترد حالة في أي طائر أليف منذ عام 2003. لا يمكن للحمام أن يصاب أو ينشر أنفلونزا الطيور.

إنفلونزا الطيور له شكل معدي جدا، ميّز أولا في إيطاليا قبل أكثر من 100 سنة، حيث كان يعرف بطاعون الطيور. إنفلونزا الطيور إذن هو مرض فيروسي يصيب الحيوانات عموما والطيور بشكل خاص. تكمن الفيروس في دماء الطيور ولعابها وأمعائها وأنوفها فتخرج في برازها الذي يجف ليتحول إلى ذرات غبار متطايرة يستنشقها الدجاج والإنسان القريب من الدجاج. ويعتبر الوز والحبش والبط والدجاج هم الأكثر إصابة لهذا الفيروس.

العوامل الوراثية

العوامل الوراثية في التمييز بين "فيروسات الأنفلونزا البشرية" و "فيروسات أنفلونزا الطيور" تشمل ما يلي:

• PB2 ( إنزيم RNA البلمرة) : مواقع الأحماض الأمينية ( أو رواسب وبقايا الأحماض الأمينية ) في موقع 627 في البروتين PB2 المشفر بواسطة جين PB2 RNA. كل فيروسات أنفلونزا الطيور H5N1 ترتبط بشيفرة الحمض الأميني -Glu- حمض الغلوتاميك (Glutamic acid) في موقع 627 في البروتين بينما كل فيروسات الأنفلونزا البشرية ترتبط بشيفرة الحمض الأميني (Lysine) في ذلك الموقع.

• هيماجلوتينين (Hemagglutinin) : فيروسات أنفلونزا الطيور HA ترتبط بمستقبلات الحمض اللعابي (sialic acid receptors) برابطة ألفا 2-3 (alpha 2-3). أما فيروسات الأنفلونزا البشرية فترتبط بمستقبلات الحمض اللعابي برابطة ألفا 2-6 (alpha 2-6). إن فيروسات أنفلونزا الخنازير لها القدرة على ربط هذين النوعين من مستقبلات الحمض اللعابي. يعتبر الهيماجلوتينين المولد المضاد الرئيسي(Antigen)الرئيسي لإنتاج الأجسام المضادة للفيروسات. ترتبط أوبئة فيروس الأنفلونزا بالتغيرات التي تحدث لهيكل المولد المضاد (Antigen) الخاص بها. وهذا مستمد أصلاً من الخنازير, وينبغي من الناحية التقنية أن يشار إليها باسم "أنفلونزا الخنازير".

خصائص الفيروس المسبب لأنفلونزا الطيور

يعيش الفيروس في أجواء باردة فقد تستطيع الاستمرار في الجو تحت درجة منخفضة مدة ثلاثة أشهر أما في الماء فتستطيع أن تعيش مدة أربعة أيام تحت تأثير درجة حرارة 22 درجة وإذا كانت الحرارة منخفضة جدا تستطيع العيش أكثر من 30 يوما. يموت الفيروس تحت تأثير درجة حرارة عالية (30 إلى 60 درجة) وقد أثبتت الدراسات أن غرام واحد من السماد الملوث كاف لأصابة مليون طير فهناك أكثر من 15 نوعا لهذا الفيروس لكن خمسة منهم قد اكتشف واثن الفم وفي الغائط، مما يسهّل انتشارا أكثر. على خلاف الدجاج، وإن البط معروف بمقاومة الفيروس حيث يعمل كناقل بدون الإصابة بأعراض الفيروس، وهكذا يساهم في انتشار أوسع.

الأنواع

يصيب فيروس إنفلونزا الطيور عادة الطيور والخنازير. ولكن منذ عام 1959م، الأنواع الفرعية من الفيروس إتش5, إتش7، وإتش9 عبرت حواجز الأنواع وأصابت البشر في 10 مناسبات. معظم فيروسات إنفلونزا الطيور تؤثّر على البشر مسببة أعراض ومشاكل تنفسية معتدلة، باستثناء مهم واحد: سلسلة إتش5إن1 (H5N1). إتش5إن1 سبّب إصابات حادّة بنسبة ضحايا مرتفعة في 1997, 2003، و2004.

أظهرت الدراسات التي تقارن عينات الفيروس مع مرور الوقت بأنّ إتش5إن1 أصبح تدريجيا مسبّبا خطيرا للمرض لدى الثديات، وأصبح أكثر قوة الآن من الماضي، حيث يستطيع الصمود لأيام أكثر في البيئة. تظهر النتائج بأنّ إتش5إن1 يوسّع مدى أستهادفه لأنواع الثديات. في 2004, إتش5إن1 سبّب مرض قاتل بصورة طبيعية للقطط الكبيرة (النمور والفهود) وأصاب تحت ظروف مخبرية القطط المنزلية، وهي أنواع لم تكن تعتبر معرّضة لأمراض ناتجة عن أيّ فيروس إنفلونزا أي.

إن حالات التفشّي الأخيرة لفيروس إنفلونزا الطيور (إتش5إن1) في الدواجن في آسيا ومصر التي تعد موطن للمرض رفع المخاوف حول مصدر العدوى وخطر إصابة البشر.

يوجد انواع مختلفة لانفلونزا الطيور، لكن هناك سلالات مكونة من 5 انواع ثانوية عرف عنها انها قد تصيب الانسان مثل h5n1/ h7n3/ h7n7/h9n7. على الاقل اصيب انسان واحد باحدى هذه السلالات ففي مقاطعة جيانغش في ديسمبر 2013 توفيت امرأة كبيرة في السن نتيجة التهاب رئوي ناتج عن اصابتها بسلالة h10n8. ولقد كانت أول ضحايا هذه السلالة. اغلب حالات المصابين بانفلونزا الطيىور كانت نتيجة لتعامل الاشخاص مع طيور نافقة نتيجة اصابتها أو جراء الاحتكاك بسوائل تحوي الفايروس، كما ويمكن أن ينتشر المرض من خلال الاسطح والفضلات ( الروث) الملوثة. وفي تصاب معظم الطيور البرية بفيروس h5n1 بشكل بسيط، في حين ان اصابة الطيور المنزلية مثل الدجاج والديك الرومي بهذا الفايروس قد تكون مميتة وأكثر فتكا لأن الطيور المنزلية أكثر اتصالا ببعضها البعض

وتشكل الدواجن المصابة تهديد كبير في أسيا بسبب انخفاض شروط النظافة وبسبب قرب الدواجن من الأحياء السكنية. وبالرغم من سهولة التقاط البشر للعدوى عن طريق الطيور الا ان انتقال العدوى بين البشر أكثر صعوبة خصوصا عند عدم تواصلهم لفترة طويلة. ومع ذلك فأن المسؤولين في مجال الصحة العامة قلقون من أن تتطور سلالات انفلونزا الطيور وتصبح قادرة على الانتقال بسهولة بين البشر. هناك بعض من سلالات انفلونزا الطيور متواجدة في امعاء اعداد كبيرة من طيور الشاطىء والطيور المائية ولكن نادرا ما تسبب هذه السلالات العدوى. وقد يكون احتمال انتشار فايروس h5n1 من أسيا إلى أوروبا بسبب صفقات الدواجن القانونية والغير قانونية هو احتمال اقوى من احتمال كون سبب انتشار الفايروس هو هجرة الطيور البرية. ولقد اظهرت دراسة حديثة أنه لم يكن هناك ارتفاع ثانوي في الاصابات في اسيا عندما هاجرت الطيور إلى الجنوب مرة اخرى بعد تكاثرها. وبدلا عن ذلك فلقد لوحظ ان انماط العدوى انتشرت في وسائل النقل بشكل أكبر مثل سكك الحديد والطرق وحدود البلاد مما يشير إلى ان تجارة الدواجن هي السبب الاقوى لانتشار الفايروس. ولقد وجد ان هناك سلالات من انفلونزا الطيور اختفت ولم يعرف عنها انها تصيب الانسان مثل تلك السلالات التي وجدت في الولايات المتحدة خصوصا في تكساس عام 2004. اما السلالات التي تسبب المرض بشكل كبير فانها تنتشر بسرعة بين قطعان الطيور قد تؤدي إلى تدمير القطيع في 28 ساعة بينما تلك التي تسبب المرض بشكل اقل فانها قد تؤثر على إنتاج البيض ولكنها ستكون قاتله بشكل اقل من نظيرتها.

العوامل الوراثية

العوامل الوراثية في التمييز بين "فيروسات الأنفلونزا البشرية" و "فيروسات أنفلونزا الطيور" تشمل ما يلي:

• PB2 ( إنزيم RNA البلمرة) : مواقع الأحماض الأمينية ( أو رواسب وبقايا الأحماض الأمينية ) في موقع 627 في البروتين PB2 المشفر بواسطة جين PB2 RNA. كل فيروسات أنفلونزا الطيور H5N1 ترتبط بشيفرة الحمض الأميني -Glu- حمض الغلوتاميك (Glutamic acid) في موقع 627 في البروتين بينما كل فيروسات الأنفلونزا البشرية ترتبط بشيفرة الحمض الأميني (Lysine) في ذلك الموقع.

• هيماجلوتينين (Hemagglutinin) : فيروسات أنفلونزا الطيور HA ترتبط بمستقبلات الحمض اللعابي (sialic acid receptors) برابطة ألفا 2-3 (alpha 2-3). أما فيروسات الأنفلونزا البشرية فترتبط بمستقبلات الحمض اللعابي برابطة ألفا 2-6 (alpha 2-6). إن فيروسات أنفلونزا الخنازير لها القدرة على ربط هذين النوعين من مستقبلات الحمض اللعابي. يعتبر الهيماجلوتينين المولد المضاد الرئيسي(Antigen)الرئيسي لإنتاج الأجسام المضادة للفيروسات. ترتبط أوبئة فيروس الأنفلونزا بالتغيرات التي تحدث لهيكل المولد المضاد (Antigen) الخاص بها. وهذا مستمد أصلاً من الخنازير, وينبغي من الناحية التقنية أن يشار إليها باسم "أنفلونزا الخنازير".

خصائص الفيروس المسبب لأنفلونزا الطيور

يعيش الفيروس في أجواء باردة فقد تستطيع الاستمرار في الجو تحت درجة منخفضة مدة ثلاثة أشهر أما في الماء فتستطيع أن تعيش مدة أربعة أيام تحت تأثير درجة حرارة 22 درجة وإذا كانت الحرارة منخفضة جدا تستطيع العيش أكثر من 30 يوما. يموت الفيروس تحت تأثير درجة حرارة عالية (30 إلى 60 درجة) وقد أثبتت الدراسات أن غرام واحد من السماد الملوث كاف لأصابة مليون طير فهناك أكثر من 15 نوعا لهذا الفيروس لكن خمسة منهم قد اكتشف واثن الفم وفي الغائط، مما يسهّل انتشارا أكثر. على خلاف الدجاج، وإن البط معروف بمقاومة الفيروس حيث يعمل كناقل بدون الإصابة بأعراض الفيروس، وهكذا يساهم في انتشار أوسع.

الأنواع

يصيب فيروس إنفلونزا الطيور عادة الطيور والخنازير. ولكن منذ عام 1959م، الأنواع الفرعية من الفيروس إتش5, إتش7، وإتش9 عبرت حواجز الأنواع وأصابت البشر في 10 مناسبات. معظم فيروسات إنفلونزا الطيور تؤثّر على البشر مسببة أعراض ومشاكل تنفسية معتدلة، باستثناء مهم واحد: سلسلة إتش5إن1 (H5N1). إتش5إن1 سبّب إصابات حادّة بنسبة ضحايا مرتفعة في 1997, 2003، و2004.

أظهرت الدراسات التي تقارن عينات الفيروس مع مرور الوقت بأنّ إتش5إن1 أصبح تدريجيا مسبّبا خطيرا للمرض لدى الثديات، وأصبح أكثر قوة الآن من الماضي، حيث يستطيع الصمود لأيام أكثر في البيئة. تظهر النتائج بأنّ إتش5إن1 يوسّع مدى أستهادفه لأنواع الثديات. في 2004, إتش5إن1 سبّب مرض قاتل بصورة طبيعية للقطط الكبيرة (النمور والفهود) وأصاب تحت ظروف مخبرية القطط المنزلية، وهي أنواع لم تكن تعتبر معرّضة لأمراض ناتجة عن أيّ فيروس إنفلونزا أي.

إن حالات التفشّي الأخيرة لفيروس إنفلونزا الطيور (إتش5إن1) في الدواجن في آسيا ومصر التي تعد موطن للمرض رفع المخاوف حول مصدر العدوى وخطر إصابة البشر.

يوجد انواع مختلفة لانفلونزا الطيور، لكن هناك سلالات مكونة من 5 انواع ثانوية عرف عنها انها قد تصيب الانسان مثل h5n1/ h7n3/ h7n7/h9n7. على الاقل اصيب انسان واحد باحدى هذه السلالات ففي مقاطعة جيانغش في ديسمبر 2013 توفيت امرأة كبيرة في السن نتيجة التهاب رئوي ناتج عن اصابتها بسلالة h10n8. ولقد كانت أول ضحايا هذه السلالة. اغلب حالات المصابين بانفلونزا الطيىور كانت نتيجة لتعامل الاشخاص مع طيور نافقة نتيجة اصابتها أو جراء الاحتكاك بسوائل تحوي الفايروس، كما ويمكن أن ينتشر المرض من خلال الاسطح والفضلات ( الروث) الملوثة. وفي تصاب معظم الطيور البرية بفيروس h5n1 بشكل بسيط، في حين ان اصابة الطيور المنزلية مثل الدجاج والديك الرومي بهذا الفايروس قد تكون مميتة وأكثر فتكا لأن الطيور المنزلية أكثر اتصالا ببعضها البعض

وتشكل الدواجن المصابة تهديد كبير في أسيا بسبب انخفاض شروط النظافة وبسبب قرب الدواجن من الأحياء السكنية. وبالرغم من سهولة التقاط البشر للعدوى عن طريق الطيور الا ان انتقال العدوى بين البشر أكثر صعوبة خصوصا عند عدم تواصلهم لفترة طويلة. ومع ذلك فأن المسؤولين في مجال الصحة العامة قلقون من أن تتطور سلالات انفلونزا الطيور وتصبح قادرة على الانتقال بسهولة بين البشر. هناك بعض من سلالات انفلونزا الطيور متواجدة في امعاء اعداد كبيرة من طيور الشاطىء والطيور المائية ولكن نادرا ما تسبب هذه السلالات العدوى. وقد يكون احتمال انتشار فايروس h5n1 من أسيا إلى أوروبا بسبب صفقات الدواجن القانونية والغير قانونية هو احتمال اقوى من احتمال كون سبب انتشار الفايروس هو هجرة الطيور البرية. ولقد اظهرت دراسة حديثة أنه لم يكن هناك ارتفاع ثانوي في الاصابات في اسيا عندما هاجرت الطيور إلى الجنوب مرة اخرى بعد تكاثرها. وبدلا عن ذلك فلقد لوحظ ان انماط العدوى انتشرت في وسائل النقل بشكل أكبر مثل سكك الحديد والطرق وحدود البلاد مما يشير إلى ان تجارة الدواجن هي السبب الاقوى لانتشار الفايروس. ولقد وجد ان هناك سلالات من انفلونزا الطيور اختفت ولم يعرف عنها انها تصيب الانسان مثل تلك السلالات التي وجدت في الولايات المتحدة خصوصا في تكساس عام 2004. اما السلالات التي تسبب المرض بشكل كبير فانها تنتشر بسرعة بين قطعان الطيور قد تؤدي إلى تدمير القطيع في 28 ساعة بينما تلك التي تسبب المرض بشكل اقل فانها قد تؤثر على إنتاج البيض ولكنها ستكون قاتله بشكل اقل من نظيرتها.

Focus

Focus

Focus is a 2015 American romantic crime comedy-drama film written and directed by Glenn Ficarra and John Requa, starring Will Smith and Margot Robbie. The film was released on February 27, 2015 and received mixed reviews from critics but was a success at the box office, grossing a total of $159 million off its $50 million budget.

Plot

Seasoned con-man Nicky Spurgeon (Will Smith) goes to an upscale restaurant, where an inexperienced grifter, Jess Barrett (Margot Robbie), seduces him, and then pretends they've been caught by her jealous husband. When the deception fails, Nicky advises them never to lose focus when faced with unexpected situations. Nicky follows Jess, and convinces her to have a drink with him. Over drinks, he tells her the story of how his father killed his grandfather in a stand-off, explaining the tactic called a "Toledo Panic Button" which means that you shoot your partner to show you're loyal.

Jess follows Nicky to New Orleans, successful in persuading Nicky to take her under his wing, where she is also introduced to Nicky's crew as well, including the obese and profane Farhad (Adrian Martinez) and fellow con-man Horst (Brennan Brown). She picks a few pockets as a test, and soon Nicky and Jess develop a romantic relationship, upsetting Nicky, who was taught by his father to never become emotionally involved with anyone in their line of business. At the 17th Associated Football Franchise of America Championship Game at the Mercedes-Benz Superdome, Nicky gets into a round of increasingly extravagant bets with gambler Liyuan Tse (B.D. Wong), eventually losing all of the money the crew has earned.

To win it back, Nicky asks Tse to pick any player on or off the field and says that Jess will guess the number picked. A distraught Jess scans the field and notices Farhad wearing jersey number 55 and realizes it is another con. They take Tse for millions of dollars. Nicky explains to Jess how Tse had been programmed to pick 55 since he arrived, with subtle, subconscious prompts throughout his day. Afterwards, Nicky, wary of his growing emotional involvement, leaves Jess by the side of the road with her cut. He instructs the driver to take her to the airport. Jess cries as her limo drives off, leaving Nicky to climb into another waiting car.

Three years later, Nicky is in Buenos Aires, working for billionaire motorsport team owner Rafael Garriga (Rodrigo Santoro). Garriga needs to beat a team headed by Australian businessman McEwen (Robert Taylor) to win the championship. Nicky will pretend to be a disgruntled technician on Garriga's team willing to sell Garriga's custom fuel use algorithm EXR. Instead he will sell McEwen a bogus version which will slow their car down during the race. At a pre-race party, Nicky runs into Jess, who is now Garriga's girlfriend. After faking heavy drinking upon seeing Jess, Nicky has a convincing fight with Garriga in public and after being thrown out, is recruited by McEwen to provide the component.

Nicky begins pursuing Jess again, and they eventually rekindle their relationship. The head of Garriga's security entourage, Owens (Gerald McRaney), is suspicious and narrowly misses catching the two together. Nicky delivers the component to McEwen for three million euros but also sells it to the other teams for similar amounts.

Nicky and Jess attempt to return to the United States together. However, they are caught by Garriga's men and taken to Garriga's garage. Jess is tied up and her mouth is taped shut whilst Nicky is given a beating. Nicky has actually sold the real EXR to all of the various teams. Garriga is convinced that Jess had something to do with Nicky gaining access to EXR and begins to suffocate the gagged Jess by holding her nose. In order to save Jess, Nicky explains that he gained access to EXR through tricking Jess into believing he still had feelings for her. That the necklace he had given to Jess was equipped to secretly record Garriga's password and login information. He explains that Jess was conned and knew nothing about this. However, Jess then reveals that she was only trying to seduce Garriga in order to steal his valuable watch and to make Nicky jealous.

Nicky promises to come clean in order to spare Jess's life but Owens shoots him in the chest, causing a horrified Garriga to leave. Owens then reveals himself to be Nicky's father, Bucky, and assures Jess that he avoided any major arteries. He simply employed the "Toledo Panic Button." Bucky then tapes up Nicky's wounds and draws excess blood out of his son's chest with a metal plunger so that he can breathe again. They flee the garage in Garriga's vehicle.

Bucky drives Nicky and Jess to the hospital to treat Nicky's punctured lung and departs with Nicky's money as a reminder of the consequences of losing focus. After he leaves, Nicky notices that Jess snatched Garriga's watch before he left the warehouse, and a smiling Nicky and Jess then go into the hospital together.

Cast

Will Smith as Nicky Spurgeon

Margot Robbie as Jess Barrett

Rodrigo Santoro as Garriga

Gerald McRaney as Bucky Spurgeon / Owens

B. D. Wong as Liyuan Tse

Robert Taylor as McEwen

Dominic Fumusa as Jared

Brennan Brown as Horst

Griff Furst as Gareth

Adrian Martinez as Farhad

Alfred Tumbley as Dogs

Billy Slaughter as Passing Thief

Juan Minujin as Barman

Stephanie Honoré as Janice

Omid Khodadad as Focus Developer

Mehdi Rafiee as CTO

Production

Apollo Robbins served as a consultant, conceiving and choreographing original sleight-of-hand maneuvers. Directors Ficarra and Requa stated, "Apollo is the foremost expert in his field and is an inspiration to us."

The directing duo and production designer Beth Mickle made a scouting trip to Buenos Aires in June and a second trip with producers Denise Di Novi and Mark Scoon, in which they finally settled to shoot in the neighborhoods of San Telmo, Puerto Madero, Barracas, Retiro, Recoleta and Palermo, as well as Ezeiza Airport and a few hotels.[5]

Neil Smith spoke at the Digital Cinema Society forum dropping several hints as to the identity of a film being edited in Final Cut Pro X in a December 2013 presentation. This would make Focus the largest production yet completed in Apple's editing program.

Filming

Principal photography began on September 14, 2013 in New Orleans, and moved over to Buenos Aires on November 19, 2013 for three weeks.[6] The last day of shooting in Argentina was on December 10.[7] Filming wrapped in New York City on December 17, 2013.[8]

Release

The film was released in 2015 in the US and Germany.[9] On January 29, 2015, WB and IMAX Corporation announced that they would digitally re-master the film into the immersive IMAX DMR format, also for release on the same date.[10]

Box office

Focus grossed $53.9 million in North America and $105.2 million in other territories for a total gross of $159.1 million, against a production budget of $50.1 million.[4]

The film grossed $6.4 million in its opening day, $7.6 million on its second day and $4.6 million on its third day, totaling $18.7 million in its opening weekend, while playing in 3,323 theaters (a $5,623 per-theatre average), finishing first place at the box office.[11] The film was also released in the theatres of 39 markets of other territories in same weekend of its North America release, and grossed an estimated $12.2 million. Its biggest territories were the United Kingdom ($13 million), Russia ($3.1 million) and Netherlands ($1,765,832).[12][13]

Critical response

Focus received mixed reviews from critics. On review aggregator website Rotten Tomatoes, the film has a rating of 57%, based on 221 reviews, with a rating average of 5.82/10. The site's consensus reads, "Focus may have a few too many twists and turns, but it nearly skates by on its glamorous setting and the charm of its stars."[14] On Metacritic, which assigns a normalized rating, the film has a score of 56 out of 100, based on 42 critics, indicating "mixed or average reviews".[15] According to CinemaScore, audiences gave the film a grade of "B" on an A+ to F scale.[16]

The Free Press Journal called the film "smart, slick, but shallow".[17]

Home media

Focus was released on DVD and Blu-ray/DVD combo pack on June 2, 2015.[18][19]

Soundtrack

The soundtrack album was released on February 24, 2015 by WaterTower Music.[20]

"I'm a Manchild" – Uptown Funk Empire

"Sofa Rockers (Richard Dorfmeister Remix)" – Sofa Surfers

"Please!" – Edward Sharpe and the Magnetic Zeros

"Wind It Up" – Stooges Brass Band

"You Don't Have to Worry" – Doris & Kelley

"Meet Me in the City" – Junior Kimbrough

"Sympathy for the Devil" - The Rolling Stones

"Gimme Danger" – The Stooges

"Chorra" – Los Mareados

"La Espada de Cadorna" – Mauro Alberelli, Fernando Diego, Barreyro, Maria Carla Flores, Fermin Echeveste, Manuel Gonzalez Aguilar, Mateo Gonzalez Aguilar and Carlos Maximiliano Russo

"Gerli Hood" – Ivan Diaz Mathe, Jorge Estenbenet, Sebastian Martinez, Francisco Olivero, Daniel Michel, Juan Manuel Meyer and Gala Iglesias Brickles featuring Camilo Costaldi Lira and Alberto Manuel Rodriguez

"Corazon de Piedra (Te Amo)" – Alenjandro Medina

"White Bird" – It's a Beautiful Day

"Love Makes the World Go Round" – Barbara Lewis

"Focus (Love Theme)" – Nick Urata

"The Windmills of Your Mind" – Ray Conniff and The Singers

الهام علي

الهام علي

إلهام علي (31 أغسطس 1985 -)، ممثلة سعودية تعيش في البحرين

حياتها

بدأت حياتها في المسرح ثم إنتقلت لتقديم برنامج مكسرات على القناة الأولى السعودية . و حاليا تعيش مع عائلتها في البحرين .