Immunoglobulin G

Immunoglobulin G (IgG) is a type of antibody. Each IgG has two antigen binding sites. Representing approximately 75% of serum antibodies in humans, IgG is the most common type of antibody found in the circulation. IgG molecules are created and released by plasma B cells.

Antibodies are major components of humoral immunity. IgG is the main type of antibody found in blood and extracellular fluid allowing it to control infection of body tissues. By binding many kinds of pathogens such as viruses, bacteria, and fungi, IgG protects the body from infection.

It does this through several mechanisms:

IgG antibodies are generated following class switching and maturation of the antibody response and thus participate predominantly in the secondary immune response. IgG is secreted as a monomer that is small in size allowing it to easily perfuse tissues. It is the only isotype that has receptors to facilitate passage through the human placenta, thereby providing protection to the fetus in utero. Along with IgA secreted in the breast milk, residual IgG absorbed through the placenta provides the neonate with humoral immunity before its own immune system develops. Colostrum contains a high percentage of IgG, especially bovine colostrum. In individuals with prior immunity to a pathogen, IgG appears about 24–48 hours after antigenic stimulation.

Therefore, in the first six months of life, the fetus has the same antibodies as the mother, till the old antibodies are then degraded and it can defend itself against all the pathogens that the mother encountered in her life (even if only through vaccination). This repertoire of immunoglobulins is crucial for the newborns who are very sensitive to infections above all for the respiratory and digestive systems.

IgG are also involved in the regulation of allergic reactions. According to Finkelman, there are two pathways of systemic anaphylaxis: antigens can cause systemic anaphylaxis in mice through classic pathway by cross-linking IgE bound the mast cell FcεRI, stimulating the release of both histamine and platelet activating factor (PAF). In the Alternative pathway antigens form complexes with IgG, which then cross-link macrophage FcγRIII and stimulates only PAF release.

IgG antibodies can prevent IgE mediated anaphylaxis by intercepting a specific antigen before it binds to mast cell –associated IgE. Consequently, IgG antibodies block systemic anaphylaxis induced by small quantities of antigen but can mediate systemic anaphylaxis induced by larger quantities.

IgG antibodies are large molecules of about 150 kDa made of four peptide chains. It contains two identical class γ heavy chains of about 50 kDa and two identical light chains of about 25 kDa, thus a tetrameric quaternary structure. The two heavy chains are linked to each other and to a light chain each by disulfide bonds. The resulting tetramer has two identical halves, which together form the Y-like shape best bpa free water bottles. Each end of the fork contains an identical antigen binding site. The various regions and domains of a typical IgG are depicted in the figure to the left. The Fc regions of IgGs bear a highly conserved N-glycosylation site. The N-glycans attached to this site are predominantly core-fucosylated diantennary structures of the complex type. In addition, small amounts of these N-glycans also bear bisecting GlcNAc and α-2,6-linked sialic acid residues.

There are four IgG subclasses (IgG1, 2 how to tenderise meat, 3, and 4) in humans, named in order of their abundance in serum (IgG1 being the most abundant).

Note: IgG affinity to Fc receptors on phagocytic cells is specific to individual species from which the antibody comes as well as the class. The structure of the hinge regions (region 6 in the diagram) contributes to the unique biological properties of each of the four IgG classes. Even though there is about 95% similarity between their Fc regions, the structure of the hinge regions is relatively different.

Given the opposing properties of the IgG subclasses (fixing and failing to fix complement; binding and failing to bind FcR), and the fact that the immune response to most antigens includes a mix of all four subclasses, it has been difficult to understand how IgG subclasses can work together to provide protective immunity. Recently the Temporal Model of human IgE and IgG function was proposed. This model suggests that IgG3 (and IgE) appear early in a response. The IgG3, though of relatively low affinity, allows IgG-mediated defences to join IgM-mediated defences in clearing foreign antigens. Subsequently, higher affinity IgG1 and IgG2 are produced safest reusable water bottle. The relative balance of these subclasses, in any immune complexes that form, helps determine the strength of the inflammatory processes that follow. Finally, if antigen persists, high affinity IgG4 is produced, which dampens down inflammation by helping to curtail FcR-mediated processes.

The relative ability of different IgG subclasses to fix complement may explain why some anti-donor antibody responses do harm a graft after organ transplantation.

In a mouse model of autoantibody mediated anemia using IgG isotype switch variants of an anti erythrocytes autoantibody, it was found that mouse IgG2a was superior to IgG1 in activating complement. Moreover, it was found that the IgG2a isotype was able to interact very efficiently with FcgammaR. As a result, 20 times higher doses of IgG1, in relationship to IgG2a autoantibodies, were required to induce autoantibody mediated pathology. It is important to remember that mouse IgG1 and human IgG1 are not necessarily similar in function, and the inference of human antibody function from mouse studies must be done with great care. Nevertheless, it remains true that both human and mouse antibodies have different abilities to fix complement and to bind to Fc receptors.

The measurement of immunoglobulin G can be a diagnostic tool for certain conditions, such as autoimmune hepatitis, if indicated by certain symptoms. Clinically, measured IgG antibody levels are generally considered to be indicative of an individual’s immune status to particular pathogens. A common example of this practice are titers drawn to demonstrate serologic immunity to measles, mumps, and rubella (MMR) rare football shirts, hepatitis B virus, and varicella (chickenpox), among others.

Testing of IgG is not indicated for diagnosis of allergy.

IgG antibodies are extracted from donated blood plasma and used as a therapeutic known as intravenous immunoglobulin therapy (IVIG). This is used to treat immune deficiencies, autoimmune disorders, and infections.

Prusias II of Bithynia

Prusias II Cynegus (Greek: Προυσίας ὁ Κυνηγός; “the Hunter”, lived c. 220 BC – 149 BC, reigned c. 182 BC – 149 BC) was the Greek king of Bithynia. He was the son and successor of Prusias I and Apama III.

Prusias was born to Prusias I and Apama III in 220 BC. His father died in 189 BC, at which point became the king of Bithynia. Prusias joined with the king of Pergamon, Eumenes II in a war against King Pharnaces I of Pontus (181–179 BC). He later invaded the territories of Pergamon (156–154 BC), only to be defeated, and the Pergamenes insisted on heavy reparations, which included 500 talents and “twenty decked ships”. Prusias married his maternal cousin Apame IV, a sister of Perseus of Macedon and a princess from the Antigonid dynasty, by whom he had a son called Nicomedes II and a daughter, also called Apama stainless steel reusable water bottle, who married Dyegilos, son of Cotys IV, King of Thrace, and wife Semestra.

Prusias was praised by the Aetolians on account of his behavior and benefactions towards them.

Towards the end of his life, Prusias II had children by a later wife, and wanted to make them his heirs in place of Nicomedes. He sent Nicomedes to Rome to ask its help in reducing the amount of these reparations, and directed the co-ambassador, Menas, to kill Nicomedes if the mission was unsuccessful. Despite the failure of the mission, Nicomedes persuaded Menas to betray Prusias, and Nicomedes declared himself king. Prusias had to renounce the kingship in favor of his son and ended up being murdered himself instead in 149 BC how to tenderise meat.

Down Under (chanson)

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Singles de Men at Work

Down Under (ou Land Down Under) est une chanson du groupe australien Men at Work sortie en single en octobre 1981, extraite de l’album Business as Usual electric tenderizer.

C’est un des plus grands succès du groupe. Il a été classé no 1 en Australie, en Nouvelle-Zélande et dans plusieurs pays d’Europe. La chanson est restée populaire, et est parfois considérée comme un « hymne officieux » de l’Australie.

Le titre devient aussi un tube en Amérique du Nord où il ne sort qu’en 1982. Il se classe en tête des charts canadiens et atteint la première place du Billboard Hot 100 aux États-Unis en janvier 1983. Il est no 4 de l’année 1983.

Une première version a été enregistrée en 1980. Elle figure en face B du premier single du groupe, Keypunch Operator, sorti en nombre très limité. La chanson n’a rencontré le succès que lors de la sortie sur l’album Business as Usual.

En 2009, l’éditeur Larrakin Music qui avait les droits sur une chanson pour enfants appelée Kookaburra fait un procès pour plagiat d’une partie de la mélodie jouée à la flûte, ce qui a profondément affecté Greg Ham qui avait affirmé avoir improvisé cette mélodie cheap football uniforms.

Colin Hay, ayant continué une carrière en solo, a repris la chanson en acoustique sur son album Man @ Work de 2003.

2016–17 UEFA Champions League

The 2016–17 UEFA Champions League is the 62nd season of Europe’s premier club football tournament organised by UEFA, and the 25th season since it was renamed from the European Champion Clubs’ Cup to the UEFA Champions League.

The 2017 UEFA Champions League Final will be played at the Millennium Stadium in Cardiff, Wales.

The winners of the 2016–17 UEFA Champions League will qualify as the UEFA representative at the 2017 FIFA Club World Cup in the United Arab Emirates, and also earn the right to play against the winners of the 2016–17 UEFA Europa League in the 2017 UEFA Super Cup.

Real Madrid are the defending champions.

A total of 78 teams from 53 of the 55 UEFA member associations are expected to participate in the 2016–17 UEFA Champions League (the exceptions being Liechtenstein, which does not organise a domestic league, and Kosovo, whose participation was not accepted in their first attempt as UEFA members). The association ranking based on the UEFA country coefficients is used to determine the number of participating teams for each association:

For the 2016–17 UEFA Champions League, the associations are allocated places according to their 2015 UEFA country coefficients, which takes into account their performance in European competitions from 2010–11 to 2014–15.

Apart from the allocation based on the country coefficients, associations may have additional teams participating in the Champions League, as noted below:

In the default access list, the Champions League title holders enter the group stage. However, since Real Madrid already qualified for the group stage (as the runners-up of the 2015–16 La Liga), the Champions League title holders berth in the group stage is given to the Europa League title holders, Sevilla.

League positions of the previous season shown in parentheses, except Sevilla which qualified as Europa League title holders (TH: Champions League title holders; EL: Europa League title holders).

The schedule of the competition is as follows (all draws are held at the UEFA headquarters in Nyon, Switzerland, unless stated otherwise).

In the qualifying rounds and the play-off round, teams were divided into seeded and unseeded teams based on their 2016 UEFA club coefficients wholesale socks and underwear, and then drawn into two-legged home-and-away ties. Teams from the same association could not be drawn against each other.

The draws for the first and second qualifying rounds were held on 20 June 2016. The first legs were played on 28 June, and the second legs were played on 5 and 6 July 2016 indoor goalkeeper gloves.

The first legs were played on 12 and 13 July, and the second legs were played on 19 and 20 July 2016.

The third qualifying round was split into two separate sections: Champions Route (for league champions) and League Route (for league non-champions). The losing teams in both sections entered the 2016–17 UEFA Europa League play-off round.

The draw for the third qualifying round was held on 15 July 2016. The first legs were played on 26 and 27 July, and the second legs were played on 2 and 3 August 2016.

The play-off round was split into two separate sections: Champions Route (for league champions) and League Route (for league non-champions). The losing teams in both sections entered the 2016–17 UEFA Europa League group stage.

The draw for the play-off round was held on 5 August 2016. The first legs were played on 16 and 17 August, and the second legs were played on 23 and 24 August 2016.

The draw for the group stage was held on 25 August 2016, at the Grimaldi Forum in Monaco. The 32 teams were drawn into eight groups of four, with the restriction that teams from the same association could not be drawn against each other. For the draw, the teams were seeded into four pots based on the following principles (introduced starting 2015–16 season):

In each group, teams play against each other home-and-away in a round-robin format. The group winners and runners-up advance to the round of 16, while the third-placed teams enter the 2016–17 UEFA Europa League round of 32. The matchdays are 13–14 September, 27–28 September, 18–19 October, 1–2 November, 22–23 November, and 6–7 December 2016.

The youth teams of the clubs that qualify for the group stage also play in the 2016–17 UEFA Youth League on the same matchdays, where they compete in the UEFA Champions League Path (the youth domestic champions of the top 32 associations compete in a separate Domestic Champions Path until the knockout phase).

A total of 17 national associations are represented in the group stage. Leicester City and Rostov made their debut appearances in the group stage.

In the knockout phase, teams play against each other over two legs on a home-and-away basis, except for the one-match final. The mechanism of the draws for each round is as follows:

The draw for the round of 16 was held on 12 December 2016. The first legs were played on 14, 15, 21 and 22 February, and the second legs were played on 7, 8, 14 and 15 March 2017.

The draw for the quarter-finals was held on 17 March 2017. The first legs will be played on 11 and 12 April, and the second legs will be played on 18 and 19 April 2017.

The draw for the semi-finals will be held on 21 April 2017. The first legs will played on 2 and 3 May, and the second legs will be played on 9 and 10 May 2017.

The final will played on 3 June 2017 at the Millennium Stadium in Cardiff, Wales. The “home” team (for administrative purposes) will be determined by an additional draw held after the semi-final draw.

Statistics exclude qualifying rounds and play-off round.

Note: Players and teams in bold are still active in the competition.

Source:

Deutsche Fußball-Amateurmeisterschaft 1991

Deutscher Fußball-Amateurmeister 1991 wurden die Amateure von Werder Bremen. Im Finale im Ludwigsburger Ludwig-Jahn-Stadion siegten sie am 9. Juni 1991 mit 2:1 gegen die gastgebende SpVgg 07 Ludwigsburg. Die Vizemeister der acht Oberligastaffeln trugen den Wettbewerb erstmals in einer nach Nord und Süd aufgeteilten Vorrunde aus, deren Gruppensieger dann im Endspiel aufeinander trafen. Zuvor wurde die deutsche Amateurmeisterschaft im K.-o.-System ausgespielt.

Die Meister der acht Oberligen und der Zweite der Oberliga Nord aus der Saison 1990/91, spielten in einer Aufstiegsrunde, die zwei Aufsteiger für die 2. Bundesliga aus. Sieben Vizemeister und der Dritte der Oberliga Nord nahmen am Wettbewerb um die deutsche Amateurmeisterschaft teil.


Kicker-Sportmagazin: Jahrgang 1991, Olympia-Verlag GmbH,

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Oberligen:  Baden-Württemberg | Bayern | Berlin | Hessen | Nord | Nordrhein | Südwest | Westfalen

Pokalwettbewerbe: DFB-Pokal&nbsp football clothes online;| FDGB-Pokal | Verbandspokale

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Barleria cristata

Barleria cristata (Philippine violet, bluebell barleria or crested Philippine violet), is a plant of the Acanthaceae family.

It is native to a wide area ranging from Southern China to India and Myanmar.

Cultivated as an ornamental plant in villages and gardens, it has become naturalized in Hawaii, where it grows in dry habitats. In Fiji, where it is known as “tombithi” and in Christmas Island (Indian Ocean), the shrub grows also as a ruderal species along roadsides and disturbed areas from near sea level to about 100 m.

It grows as a shrub 60 –100 cm tall. The leaves are dark green on the upper surface and pale green on the lower surface. They are elliptic to narrowly ovate. The flowers are about 5 cm long, funnel-shaped in violet, pink, or white color. The fruits are about 1.5 cm long ellipsoid capsules. Thy become glabrous and glossy at maturity.

in Narsapur, Medak district, India

in Narsapur, Medak district, India

Barleria cristata shrub.

in Narsapur, Medak district, India

in Narsapur, Medak district, India

at Ananthagiri Hills, in Rangareddy district of Andhra Pradesh, India clear water bottles.

at Ananthagiri Hills, in Rangareddy district of Andhra Pradesh, India.

at Ananthagiri Hills, in Rangareddy district of Andhra Pradesh, India.

at Ananthagiri Hills, in Rangareddy district of Andhra Pradesh, India.

at Mastyagiri, Nalgonda District of Andhra Pradesh, India.

Known as อังกาบ how to tenderise meat, this plant is used in Thailand as a traditional herbal remedy. It allegedly acts as a tonic, diuretic and blood purifier professional football jerseys.[citation needed]

In Tamil Nadu in South India, it is known as December Poo or December Flower as it blooms in December and is normally strung into garlands of flowers for women to wear in their hair.[citation needed]