title: Protectin D1

abstract: Protectin D1 also known as neuroprotectin D1 and abbreviated most commonly as PD1 or NPD1 is a member of the class of specialized proresolving mediators. Like other members of this class of polyunsaturated fatty acid metabolites, it possesses strong anti-inflammatory, anti-apoptotic and neuroprotective activity. PD1 is an aliphatic acyclic alkene 22 carbons in length with two hydroxyl groups at the 10 and 17 carbon positions and one carboxylic acid group at the one carbon position. Specifically, PD1 is an endogenous stereoselective lipid mediator classified as an autocoid protectin. Autacoids are enzymatically derived chemical mediators with distinct biological activities and molecular structures. Protectins are signaling molecules that are produced enzymatically from unsaturated fatty acids. Their molecular structure is characterized by the presence of a conjugated system of double bonds. PD1, like other protectins, is produced by the oxygenation of the ω-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) and it is found in many tissues, such as the retina, the lungs and the nervous system. PD1 has a significant role as an anti-inflammatory, anti-apoptotic and neuroprotective molecule. Studies in Alzheimer's disease animal models, in stroke patients and in human retina pigment epithelial cells (RPE) have shown that PD1 can potentially reduce inflammation induced by oxidative stress and inhibit the pro-apoptotic signal, thereby preventing cellular degeneration. Finally, recent studies examining the pathogenicity of influenza viruses, including the avian flu (H5N1), have suggested that PD1 can potentially halt the proliferation of the virus, thus protecting respiratory cells from lethal viral infections.

text:
# Protectin D1

**Protectin D1** also known as **neuroprotectin D1** (when it acts in the nervous system) and abbreviated most commonly as PD1 or NPD1 is a member of the class of specialized proresolving mediators. Like other members of this class of polyunsaturated fatty acid metabolites, it possesses strong anti-inflammatory, anti-apoptotic and neuroprotective activity. PD1 is an aliphatic acyclic alkene 22 carbons in length with two hydroxyl groups at the 10 and 17 carbon positions and one carboxylic acid group at the one carbon position.

Specifically, PD1 is an endogenous stereoselective lipid mediator classified as an autocoid protectin. Autacoids are enzymatically derived chemical mediators with distinct biological activities and molecular structures. Protectins are signaling molecules that are produced enzymatically from unsaturated fatty acids. Their molecular structure is characterized by the presence of a conjugated system of double bonds. PD1, like other protectins, is produced by the oxygenation of the ω-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) and it is found in many tissues, such as the retina, the lungs and the nervous system.

PD1 has a significant role as an anti-inflammatory, anti-apoptotic and neuroprotective molecule. Studies in Alzheimer's disease animal models, in stroke patients and in human retina pigment epithelial cells (RPE) have shown that PD1 can potentially reduce inflammation induced by oxidative stress and inhibit the pro-apoptotic signal, thereby preventing cellular degeneration. Finally, recent studies examining the pathogenicity of influenza viruses, including the avian flu (H5N1), have suggested that PD1 can potentially halt the proliferation of the virus, thus protecting respiratory cells from lethal viral infections.

## Biosynthesis of PD1

In vivo, PD1 is mainly produced as a response to inflammatory signals and it is found in various tissues, such as the retina pigment epithelial cells, lung epithelial cells, peripheral blood mononuclear cells (PBMC) and neural tissues. Studies in PBMC have shown that endogenous DHA, the main precursor of PD1, is released by the activity of phospholipase A2. According to these studies, PD1 is preferentially synthesized in PBMC cells skewed to the Type 2 T helper cell phenotype (TH2). This suggests that T-cell differentiation plays an important role in the activation of the PD1 biosynthetic pathway. The interaction of PBMC with interleukin 4 (IL-4), a potent inflammatory signal, leads to the differentiation of PBMC to TH2 type lymphocytes. In addition, activated TH2 cells further release IL-4, leading to the up-regulation of the enzyme 15-lipoxygenase-1 (15-LO-1). 15-LO-1 is a non-heme iron-carrying dioxygenase that adds oxygen atoms in a stereospecific manner on free and esterified ω-3 polyunsaturated fatty acids like DHA. Overall, the biosynthesis of PD1 proceeds through three distinct steps throughout which the activity of 15-LO-1 is essential. In the first step of the biosynthetic pathway, the binding of 15-LO-1 to its substrate (DHA) leads to the formation of the (17*S*)-hydro(peroxy)-DHA intermediate. This intermediate is rapidly processed to form a 16(17)-epoxide-containing molecule, which is the second intermediate. Finally, in the third step of the pathway, enzymatic hydrolysis of the 16(17)-epoxide-containing intermediate leads to the formation of PD1.

## Functions of PD1

In general, PD1 in vivo exhibits a potent anti-apoptotic and anti-inflammatory activity in the tissues in which it is localized. DHA, the main PD1 precursor, is mostly found in tissues such as the retinal synapses, photoreceptors, the lungs and the brain, suggesting that these tissues are more likely to be benefited from the protecting activity of PD1.

### Activity of PD1 in the retina

RPE are essential in the survival and renewal of the photoreceptors in the retina. These cells exhibit a potent phagocytic activity that ensures the proper function of the retina. Therefore, oxidative stress can potentially damage the RPE cells and cause vision impairment. Studies in human RPE cells have suggested that the presence of oxidative stress triggering molecules, such as H2O2 causes the fragmentation of the DNA that in turn triggers apoptosis. These studies have proposed that PD1 acts as a signaling molecule and through its ligand-receptor interaction down-regulates the expression of genes, such as the transcription factor NF-κB. The inhibition of NF-κB results in the down-regulation of the pro-inflammatory gene COX-2 (cyclooxygenase-2) which is responsible for the release of prostaglandins, a potent pro-inflammatory mediator. In addition, PD1 has an important role in regulating the expression of the Bcl-2 family proteins (Bcl-2, Bcl-xL, Bax and Bad) that precedes the release of the cytochrome c complex from the mitochondria and the formation of the apoptosome. The presence of PD1 up-regulates the expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL, while it inhibits the expression of the pro-apoptotic proteins Bax and Bad. Specifically, PD1 regulates this protein family by promoting the dephosphorylation of Bcl-xL by protein phosphatase 2A (PP2A) at residue Ser-62 which in turn heterodimerizes with the pro-apoptotic protein Bax and inactivates it. Consequently, the activity of the Bcl-2 family proteins results in the inhibition of the caspase 3 enzyme, thus preventing apoptosis and promoting RPE cell survival.

### Effects of PD1 in Alzheimer's disease

Among others, Alzheimer's disease is characterized by the reduced concentration of PD1 and by the increased concentration of the amyloid-β peptide (Aβ42) that is responsible for the formation of senile plaques and also induces inflammation and apoptosis in neuronal tissues. Aβ42 is generated by the enzymatic cleavage of the β-amyloid precursor protein (βΑPP) through β- and γ- secretases. Like other pro-inflammatory mediators, Aβ42 induces inflammation through the activation of the pro-inflammatory enzyme COX-2 and the release of prostaglandins. Moreover, the release of Aβ42 down-regulates the anti-apoptotic proteins Bcl-2 and Bcl-xL and up-regulates the pro-apoptotic proteins Bax and Bad that ultimately lead to the formation of the apoptosome. PD1 in human neuronal glial cells (HNG) has been shown to trigger the down-regulation of βΑPP, thus decreasing the Aβ42 content in neuronal tissues and reducing inflammation and apoptosis. Specifically, PD1 in Alzheimer's disease models has been shown to respond to the increased concentration of the pro-inflammatory molecule Aβ42 by binding and activating the peroxisome proliferator-activated receptor gamma (PPARγ) either directly or via other mechanisms. According to some models the activation of PPARγ leads to increased ubiquitination and degradation of βAPP, thus reducing the release of Aβ42. Furthermore, PD1 inhibits the production of Aβ42 peptide by down-regulating β-secretase-1 (BACE1), while up-regulating the α-secretase ADAM10 and the secreted amyloid precursor protein-α (sAPPα). Overall, the above mechanism leads to the cleavage of βAPP protein though a non-amyloidogenic pathway that halts the formation of Aβ42 and prevents the premature neuronal degeneration.

### Antiviral activity of PD1

Studies in cultured human lung epithelial cells infected with the influenza virus H1N1 or H5N1 have found that endogenous production of PD1 decreases dramatically during infection due to the inhibition of 15-LO-1. Furthermore, the same studies have shown that in vivo administration of PD1 to H1N1 infected mice can potentially inhibit both the proliferation of the virus and the inflammation caused by the infection, thus increasing survival. PD1 protects against viral infections by disrupting the virus life cycle. Specifically, PD1 inhibits the binding of viral RNA to specific nuclear export factors in the host cells, thus blocking the export of viral RNA from the nucleus to the cytosol. The nuclear RNA export factor 1(NXF1) is of particular interest in the attenuation of viral infections via the activity of PD1. Specifically, the NXF1 transporter through its middle and C-terminal domains binds to the phenylalanine/glycine repeats in the nucleoporins (Nups) that line the nuclear pore. In the absence of PD1, influenza viral RNA binds to the NXF1 transporter that later binds specifically to Nup62 nucleoporin and exports the viral RNA into the cytosol. However, the administration of PD1 has shown that this lipid mediator specifically inhibits the binding of the viral RNA to NXF1, thus disrupting the proliferation of the virus.

## Laboratory Synthesis of PD1

The large scale industrial production of PD1 is of great interest for pharmaceutical companies in order to harvest the potent anti-inflammatory and anti-apoptotic activities of this lipid mediator. So far, very few stereoselective laboratory syntheses of PD1 have been reported, but with a relatively low yield.

### Convergent Stereoselective Synthesis

According to one method, PD1 is synthesized in 15% yield through an 8-step convergent stereoselective process. Initially, the alkyne, (*Z*)-3-tertbutyldimethylsiloxy-oct-5-en-1-yne reacts with bromo-*E*,*E*,*Z*,*Z*-tetraene ester in a Sonogashira cross-coupling reaction at room temperature in the presence of Pd-(PPh3)4 and CuI using diethylamine as a solvent which produces the bis-hydroxyl-protected methyl ester. Removal of the two tert-butyldimethylsilyl ethers (TBS-protecting groups) is attained with an excess of TBAF in THF at 0 °C which produces a diol containing a conjugated alkyne. The conjugated alkyne is reduced to the methyl ester. In addition, the diol is hydrogenated using the Lindlar catalyst, with 1-octene added as a sacrificial olefin, to produce a highly stereoselective triene, while water is eliminated from the diol through a Boland reduction. Finally, the methyl ester undergoes saponification at 0 °C with dilute LiOH (aq.) in methanol followed by acidic work-up with NaH2PO4 (aq.) in order to produce PD1.

### Alternative Stereoselective Synthesis

Alternatively, PD1 laboratory synthesis proceeds through a different stereoselective method. Initially, hydroboration of a TBS-protected acetylene with Sia2BH produces a TBS-protected vinylborane. The TBS-protected vinylborane reacts with vinyliodide in the presence of a Pd-catalyst, sodium hydroxide (NaOH) and THF to produce a TBS-protected alcohol. Later treatment of the TBS-protected alcohol with TBAF removes the protecting group and produces a diol. Finally, the diol is hydrolyzed with LiOH in THF (aq.) to produce PD1.

## Other PDs

### 22-hydroxy-NPD1

22-hydroxy-PD1 (22-OH-PD1; i.e. 10*R*,17*S*,20-trihydroxy-4*Z*,7*Z*,11*E*,13*E*,15*Z*,19*Z*-docosahexaenoic acid) is an omega oxidation product of PD1 probably formed in cells by the action of an unidentified Cytochrome P450 omega hydroxylase (see specialized proresolving mediators#Protectins/neuroprotectins). While the omega oxidation of many bioactive fatty acid metabolites such as leukotriene B4, 5-HETE, 5-oxo-eicosatetraenoic acid (i.e. 5-oxo-ETE) results in a ~100-fold fall in their activity, the omega oxidized product of PD1 has been shown to possess potent ease exhibits potent anti-inflammatory and proresolving actions by inhibiting PMN chemotaxis in vivo and in vitro and decreased pro-inflammatory mediator levels in inflammatory exudates of an animal model at levels comparable to PD1.

### Protectin DX

Protectin DX (PDX; i.e. 10*S*,17*S*-dihydroxy-4*Z*,7*Z*,11*E*,13*Z*,15*E*,19*Z*-docosahexaenoic acid) is the 13*Z*,15*E*,19*Z* isomer of NPD1 (which has the 13*E*,15*Z*,19*Z* double bond configuration)(see specialized proresolving mediators#Protectins/neuroprotectins). An early study mistakenly used PDX instead of PD1 in attributing anti-replicative and clinically beneficial effects in viral influenza disease in a mouse model to PD1. PDX also inhibits influx of circulating leukocytes into the peritoneum in a mouse model of inflammation. PDX has other anti-inflammatory actions. It inhibits COX-1 and COX-2 thereby blocking the formation of pro-inflammatory prostaglandins; it also inhibits the platelet-aggregating action of thromboxane A2 thereby blocking the platelet aggregations responses to agents that depend on platelets to release thromboxane A2.

### Aspirin-triggered PD1

Aspirin-triggered PD1 (AT-PD1 or 17-epi-PD1: i.e. 10*R*,17*R*-dihydroxy-4*Z*,7*Z*,11*E*,13*E*,15*Z*,19*Z*-docosahexaenoic acid) is the 10*R*-hydroxy isomer of PD1 (which has the 10*S* hydroxy residue) (see specialized proresolving mediators#Protectins/neuroprotectins). AT-PD1 has been shown to **a)** reduce the infiltration of neutrophils into the peritoneum in a mouse model of inflammatory disease; **b)** stimulate the Efferocytosis (i.e. engulfment and removal) of neutrophils; and **c)** reduce brain infarction and stroke in a rodent model.

### 10-epi-PD1

10-Epi-PD1 (ent-AT-NPD1: i.e. 10*S*,17*S*-Dihydroxy-4*Z*,7*Z*,11*E*,13*E*,15*Z*,19*Z*-docosahexaenoic acid) is the 10*S*-hydroxy isomer of AT-PD1 (which has a 10*R*-hydroxy residue) (see specialized proresolving mediators#Protectins/neuroprotectins). 10-Epi-PD1 was detected in only a small amount in human PMN extracts but was more potent than PD1 or PDX in blocking the inflammatory response to zymosan A-induced murine acute peritonitis.

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## InfoBox

Protectin D1
|  | |
| --- | --- |
| Names | |
| Preferred IUPAC name (4*Z*,7*Z*,10*R*,11*E*,13*E*,15*Z*,17*S*,19*Z*)-10,17-Dihydroxydocosa-4,7,11,13,15,19-hexaenoic acid | |
| Other names 10R,17S-Dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoate; 10R,17S-Dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid; Neuroprotectin D1 | |
| Identifiers | |
| CAS Number |  |
| 3D model (JSmol) |  |
| ChemSpider |  |
| PubChem CID |  |
| UNII |  |
| CompTox Dashboard (EPA) |  |
| InChI * InChI=1S/C22H32O4/c1-2-3-10-15-20(23)17-12-8-9-13-18-21(24)16-11-6-4-5-7-14-19-22(25)26/h3,5-13,17-18,20-21,23-24H,2,4,14-16,19H2,1H3,(H,25,26)/b7-5-,9-8+,10-3-,11-6-,17-12-,18-13+/t20-,21+/m0/s1 YKey: CRDZYJSQHCXHEG-SFVBTVKNSA-N Y | |
| SMILES * O=C(O)CC\C=C/C/C=C\C\[C@@H\](O)\C=C\C=C\C=C/\[C@@H\](O)C\C=C/CC | |
| Properties | |
| Chemical formula | C22H32O4 |
| Molar mass | 360.4871 g/mol |
| Density | 1.049 g/cm3 |
| Boiling point | 559.379 °C (1,038.882 °F; 832.529 K) |
| Solubility in water | 0.0069 |
| log *P* | 4.95 |
| Acidity (p*K*a) | 4.82 |
| Except where otherwise noted, data are given for materials in their standard state (at 25 °C \[77 °F\], 100 kPa).  Infobox references | |


title: Finns Point Range Light

abstract: The Finns Point Range Rear Light is a lighthouse in Pennsville Township, Salem County, New Jersey. It is located just east of the Delaware River and was part of Range light pair that guided ships into the Delaware River. It is deactivated, and its lamp and lens have been removed, but the lighthouse is open to the public as part of a National Wildlife Refuge. It was designed and built in 1877 and is a classic example of a skeletal cast iron prefabricated lighthouse. Its companion Front range light was demolished and replaced with an offshore automated light in 1938. Both the Rear and replacement Front lights were deactivated in 1950.

text:
# Finns Point Range Light

The **Finns Point Range Rear Light** is a lighthouse in Pennsville Township, Salem County, New Jersey. It is located just east of the Delaware River and was part of Range light pair that guided ships into the Delaware River. It is deactivated, and its lamp and lens have been removed, but the lighthouse is open to the public as part of a National Wildlife Refuge. It was designed and built in 1877 and is a classic example of a skeletal cast iron prefabricated lighthouse. Its companion Front range light was demolished and replaced with an offshore automated light in 1938. Both the Rear and replacement Front lights were deactivated in 1950.

## InfoBox

Finns Point Range Lighthouse
| Finns Point Range Lighthouse | |
| --- | --- |
|  | |
| Location | Pennsville, New Jersey |
| Coordinates | 39°37′2″N 75°32′3″W / 39.61722°N 75.53417°W / 39.61722; -75.53417 |
| Tower | |
| Constructed | 1877 |
| Foundation | Masonry |
| Construction | Wrought Iron |
| Automated | 1934 |
| Height | 115 feet (35 m) |
| Shape | Skeletal w/cylinder |
|  | |
| Light | |
| First lit | 1877 |
| Deactivated | 1950 |
| Lens | Fourth Order Fresnel lens |
| Characteristic | 1 Second Eclipse (Currently Not Lit) |
|  | |


title: Triumph Tiger T110

abstract: The Triumph Tiger 110 is a British sports motorcycle that Triumph first made at their Coventry factory between 1953 and 1961. The T110 was developed from the Triumph Thunderbird and first appeared in 1954. Although it was supposed to be the sports model of the Triumph range, the Tiger 110 was later fitted with the rear paneling that was introduced with Triumph's 350cc 3TA twin in 1957. This rear cowling earned it the nickname 'bathtub' from its shape and made the T110 look somewhat staid. From 1959 the T120 Bonneville became Triumph's leading sports model, and before the introduction of the unit construction 650cc twin in 1962, the T110 was dropped from Triumph's range.

text:
# Triumph Tiger T110

The **Triumph Tiger 110** is a British sports motorcycle that Triumph first made at their Coventry factory between 1953 and 1961. The T110 was developed from the Triumph Thunderbird and first appeared in 1954.

Although it was supposed to be the sports model of the Triumph range, the Tiger 110 was later fitted with the rear paneling that was introduced with Triumph's 350cc 3TA twin in 1957. This rear cowling earned it the nickname 'bathtub' from its shape and made the T110 look somewhat staid. From 1959 the T120 Bonneville became Triumph's leading sports model, and before the introduction of the unit construction 650cc twin in 1962, the T110 was dropped from Triumph's range.

## Development

The Triumph Tiger 110 650 cc OHV Twin was developed for the American market, and was Triumph's fastest production motorcycle to date. The T110 was built in 1953 and introduced as a 1954 model. The originally cast iron cylinder block and head soon were replaced with a light alloy cylinder head with special airways to improve cooling and austenitic iron valve seat inserts. The external oil feed pipes were also replaced with internal oilways via the pushrod tubes.

The Triumph Tiger 100 was named because it was capable of 100 mph (160 km/h). The best one way speed obtained with the Tiger 110 by *The Motor Cycle* magazine was 109 mph (175 km/h)  although the speedometer read 114 mph (183 km/h).

By 1959, the Tiger 110 was eclipsed by the dual carburettor Bonneville T120 as Triumph's fastest model. The Tiger 110 then received the enclosed panels of the Twenty One which, resembling an upside-down Victorian slipper bathtub, earned the bike the nickname 'bathtub'.

## World Speed Record

On 6 September 1956, at Bonneville Salt Flats American racer Johnny Allen secured the motorcycle land-speed record on a heavily modified Triumph T110 with a top speed of 214.17 mph (344.67 km/h). This success led to the development of the Tiger T110's successor - the Triumph Bonneville.

## InfoBox

Triumph Tiger T110
|  | |
| --- | --- |
| Manufacturer | Triumph |
| Production | 19531961 |
| Engine | 649 cc parallel twin OHV four-stroke |
| Transmission | 4 speed / chain |
| Wheelbase | 57 inches (140 cm) |
| Seat height | 31 inches (79 cm) |
| Weight | 420 lb (190 kg) (dry)
 |
| Fuel capacity | 4 imp gal (18 L; 4.8 US gal) |
| Fuel consumption | 70 mpgimp (4.0 L/100 km; 58 mpgUS) at 60 mph (97 km/h) |


title: Värmdö Municipality

abstract: Värmdö Municipality is a municipality in Stockholm County in east central Sweden. Its seat is in the town of Gustavsberg, with a population of 9,682 (2005), on the main island at an elevation of 37 metres (121 ft). The municipality is named after the main island Värmdön, 180 km⁲ (69 sq mi) in size. The municipality in its present form was created in 1974, when "old" Värmdö was amalgamated with Gustavsberg and Djurö.

text:
# Värmdö Municipality

**Värmdö Municipality** (*Värmdö kommun*) is a municipality in Stockholm County in east central Sweden. Its seat is in the town of Gustavsberg, with a population of 9,682 (2005), on the main island at an elevation of 37 metres (121 ft).

The municipality is named after the main island Värmdön, 180 km2 (69 sq mi) in size.

The municipality in its present form was created in 1974, when "old" Värmdö was amalgamated with Gustavsberg (which had been detached from it in 1902) and Djurö.

## Geography

The municipality consists of 10,000 islands, all part of Stockholm archipelago. The larger islands are Värmdö, Ingarö, Fågelbrolandet, Djurö/Vindö, Svartsö, Möja, Granholmen, Runmarö and Nämdö. Gustavsberg is the main town, and there are also several villages and suburbs spread out such as Djurö, Stavsnäs, Mörtnäs, Hemmesta, Brunn, Strömma and Sandhamn.

## History

The name Värmdö can be traced to 1314, but it is not clear what it means. (It is likely that it comes from the word *värmd*, a small hot spring in the ocean which causes holes in the ice in winter, and which there are several of in the area.) The area has however been inhabited longer than that, probably from the Stone Age wherefrom remains are found. The people lived on fishing and the hunting of seals and sea birds. As the coast climate was not suitable for traditional cereal crops, the agricultural efforts were often directed towards the cultivation of potatoes.

After the introduction of steam boat lines around 1850, wealthy people in Stockholm started to build vacation houses around the stations. When today's main roads were built in the 1930s, only the steam boats serving islands remained, and the expansion continued. With the municipal reform in the 1970s, Värmdö was created through a merger between six small municipalities and adopted the coat of arms of Gustavsberg, with two porcelain ovens.

Värmdö is a rapidly expanding suburban area to Stockholm and also one of the most exclusive areas for vacation houses in Sweden. During the summer month, the population triples.

## Industry

The industry of the municipality was dominated by the porcelain factory in Gustavsberg, established in the 1820s. Around the year 1900, 1,000 people were employed there, making it one of the largest working places in Sweden.

During the summer the population of the municipality triples due to the large number of tourists and vacation houses.

## Demography

### Population development

Population development in Värmdö Municipality 1970–2019
| Year | Population |
| --- | --- |
| 1970 | 12,882 |
| 1975 | 16,050 |
| 1980 | 17,846 |
| 1985 | 19,173 |
| 1990 | 22,067 |
| 1995 | 26,548 |
| 2000 | 31,260 |
| 2005 | 34,933 |
| 2010 | 38,301 |
| 2015 | 41,107 |
| 2017 | 43,444 |
| 2019 | 45,000 |
| Source: SCB - Folkmängd efter region och år. | | | | | | | | | |

### 2022 by district

This is a demographic table based on Värmdö Municipality's electoral districts in the 2022 Swedish general election sourced from SVT's election platform, in turn taken from SCB official statistics.

In total there were 46,157 residents, including 33,811 Swedish citizens of voting age. 45.5% voted for the left coalition and 53.4% for the right coalition. Indicators are in percentage points except population totals and income.

### Residents with a foreign background

On 31 December 2017 the number of people with a foreign background (persons born outside of Sweden or with two parents born outside of Sweden) was 7 305, or 16.81% of the population (43 444 on 31 December 2017). On 31 December 2002 the number of residents with a foreign background was (per the same definition) 4 515, or 13.82% of the population (32 664 on 31 December 2002). On 31 December 2017 there were 43 444 residents in Värmdö, of which 5 683 people (13.08%) were born in a country other than Sweden. Divided by country in the table below - the Nordic countries as well as the 12 most common countries of birth outside of Sweden for Swedish residents have been included, with other countries of birth bundled together by continent by Statistics Sweden.

## Transport

Värmdö is more easily accessible by water than by land. The boat service Waxholmsbolaget offers routes to various islands in the Värmdö archipelago. By land, the major road is the county road 222, a motorway from Stockholm. It ends in the ferry harbour of Stavsnäs, one of the major connection points in the Stockholm archipelago.

The municipality has no rail connection, but is served by a number of bus routes operated by Storstockholms Lokaltrafik, SL. Most buses terminate in Stockholm at Slussen. In 2018, the bus terminal was moved to a temporary terminal to the east, which has a higher capacity than the old slot.

Some of the major bus lines to Värmdö include 422 from Nacka, 425, 433, 434, and 474 from Stockholm. Bus connections have improved significantly since the addition of several routes in 2005.

## Sports

The following sports clubs are in Värmdö Municipality:

## Notable people

## InfoBox

| Värmdö Municipality *Värmdö kommun* | |
| --- | --- |
| Municipality | |
|  | |
|  | |
|  | |
| Coordinates: 59°20′N 18°23′E / 59.333°N 18.383°E / 59.333; 18.383 | |
| Country | Sweden |
| County | Stockholm County |
| Seat | Gustavsberg |
| Area | |
| Total | 2,980.11 km2 (1,150.63 sq mi) |
| Land | 448.03 km2 (172.99 sq mi) |
| Water | 2,532.08 km2 (977.64 sq mi) |
|  | Area as of 1 January 2014. |
| Population (31 December 2023) | |
| Total | 46,637 |
| Density | 16/km2 (41/sq mi) |
| Time zone | UTC+1 (CET) |
| Summer (DST) | UTC+2 (CEST) |
| ISO 3166 code | SE |
| Province | Uppland and Södermanland |
| Municipal code | 0120 |
| Website | www.varmdo.se |
| Density is calculated using land area only. | |


title: WGL

abstract:
WGL may refer to:
  - WGL, the original (1927–1928) call sign of the New York City radio station that has since evolved into WADO
  - WGL (AM), a radio station licensed to Fort Wayne, Indiana
  - WGL (software) a window management interface for OpenGL on Windows platforms
  - WGL-FM, a former (2007-2014) call sign of a radio station licensed to Huntington, Indiana, which was changed to WJCI
  - WGL Holdings or its subsidiary, the Washington Gas Light Company.
  - Warragul railway station, Australia
  - Windows Glyph List 4
  - Warren, Gorham & Lamont, an American publisher owned by Thomson Reuters

text:
# WGL

**WGL** may refer to:

* WGL, the original (1927–1928) call sign of the New York City radio station that has since evolved into WADO
* WGL (AM), a radio station (1250 AM) licensed to Fort Wayne, Indiana
* WGL (software) a window management interface for OpenGL on Windows platforms
* WGL-FM, a former (2007-2014) call sign of a radio station (102.9 FM) licensed to Huntington, Indiana, which was changed to WJCI
* WGL Holdings or its subsidiary, the Washington Gas Light Company.
* Warragul railway station, Australia
* Windows Glyph List 4
* Warren, Gorham & Lamont, an American publisher owned by Thomson Reuters


title: WGLH

abstract: WGLH is a Christian radio station licensed to Hawkinsville, Georgia, broadcasting at 103.9 MHz. The station previously went by the call letters WCEH-FM, WQSY, WRPG and WQXZ. In March 2017, WQXZ was sold to Educational Media Foundation (EMF) by Georgia Eagle Media for $150,000. The station was turned off for the format change on May 5 at 6 PM. A few days later, the station returned to air broadcasting the contemporary Christian (K-Love) format. The purchase by EMF was consummated on May 10, 2017.

text:
# WGLH

**WGLH** (103.9 FM) is a Christian radio station licensed to Hawkinsville, Georgia, broadcasting at 103.9 MHz.

The station previously went by the call letters WCEH-FM, WQSY, WRPG and WQXZ.

In March 2017, WQXZ was sold to Educational Media Foundation (EMF) by Georgia Eagle Media for $150,000. The station was turned off for the format change on May 5 at 6 PM.

A few days later, the station returned to air broadcasting the contemporary Christian (K-Love) format. The purchase by EMF was consummated on May 10, 2017.

32°10′05″N 83°37′52″W / 32.168°N 83.631°W / 32.168; -83.631

## InfoBox

WGLH
|  | |
| --- | --- |
|  | |
| Frequency | 103.9 MHz |
| Programming | |
| Format | Contemporary Christian (K-Love) |
| Network | K-Love |
| Ownership | |
| Owner | Educational Media Foundation |
| History | |
| First air date | 1968 (as WCEH-FM) |
| Former call signs | WCEH-FM (1968–1993)
WQSY (1993–2004)
WRPG (2004–2008)
WQXZ (2008–2020) |
| Technical information | |
| Licensing authority | FCC |
| Facility ID | 67693 |
| Class | C3 |
| ERP | 10,500 watts |
| HAAT | 151 meters |
| Links | |
| Public license information |  |


title: Loudoun Valley Estates, Virginia

abstract: Loudoun Valley Estates is a census-designated place (CDP) in Loudoun County, Virginia, United States. The population as of the 2010 United States Census was 3,656. It is a Toll Brothers community located near the planned Ashburn Metro station complex and Moorefield Station town center in the southern part of Ashburn, Virginia. Loudoun Valley Estates is governed by a homeowners' association. It was formerly part of the county planning commission's Urban Policy Area but has been removed. The community is served by the Loudoun County Parkway.

text:
# Loudoun Valley Estates, Virginia

**Loudoun Valley Estates** is a census-designated place (CDP) in Loudoun County, Virginia, United States. The population as of the 2010 United States Census was 3,656. It is a Toll Brothers community located near the planned Ashburn Metro station complex and Moorefield Station town center in the southern part of Ashburn, Virginia. Loudoun Valley Estates is governed by a homeowners' association.

It was formerly part of the county planning commission's Urban Policy Area but has been removed. The community is served by the Loudoun County Parkway.

## Geography

Loudoun Valley Estates is in southeastern Loudoun County and is bordered by Brambleton to the south and west, Broadlands and Moorefield to the north, and the runways of Dulles International Airport to the east. It is 2 miles (3 km) southwest of the Dulles Greenway (Virginia Route 267), 11 miles (18 km) south of Leesburg, the county seat, and 32 miles (51 km) west-northwest of Washington, D.C.

According to the U.S. Census Bureau, the Loudoun Valley Estates CDP has a total area of 2.8 square miles (7.3 km2), of which 0.02 square miles (0.06 km2), or 0.76%, are water. The community is drained by Broad Run, a northeast-flowing tributary of the Potomac River.

The land around Loudoun Valley Estates is gently rolling. The average elevation is 289 feet (88 m). The population density is about 500 people per square kilometer.

The climate is humid subtropical. The average temperature is 57 °F (14 °C). The warmest month is August, at 77 °F (25 °C), and the coldest is January, at 32 °F (0 °C). The average rainfall 46.8 inches (1,188 mm) per year. The wettest month was October, at 5.0 inches (128 mm) of rain, and the least wet was November, at 2.1 inches (54 mm).

## Demographics

According to the 2010 census, Loudoun Valley Estates had a population of 3,656. Of this, 29.3% were white; 4.2% African American; 0.3% were American Indians and Alaska Natives; 61% were Asian; 0.0% Hawaiians and other Pacific Islanders; 1.1% from another race, and 4.1% from two or more races. 3.3% of the total population were Hispanic or Latino of any race.

## Notable residents

*Survivor* contestant Reem Daly lives in Loudoun Valley Estates.

## InfoBox

| Loudoun Valley Estates, Virginia | |
| --- | --- |
| Census-designated place | |
| Aerial view of the Loudoun Valley Estates | |
| Loudoun Valley EstatesLoudoun Valley EstatesLoudoun Valley Estates | |
| Coordinates: 38°58′51″N 77°30′28″W / 38.98083°N 77.50778°W / 38.98083; -77.50778 | |
| Country | United States |
| State | Virginia |
| County | Loudoun |
| Area | |
| Total | 2.83 sq mi (7.32 km2) |
| Land | 2.81 sq mi (7.27 km2) |
| Water | 0.02 sq mi (0.06 km2) |
| Elevation | 295 ft (90 m) |
| Population (2010) | |
| Total | 3,656 |
| Density | 1,303/sq mi (503.2/km2) |
| Time zone | UTC−5 (Eastern (EST)) |
| Summer (DST) | UTC−4 (EDT) |
| ZIP codes | 20148 (Ashburn)
20166 (Sterling) |
| FIPS code | 51-47136 |
| GNIS feature ID | 2584868 |


title: Methylation

abstract: Methylation, in the chemical sciences, is the addition of a methyl group on a substrate, or the substitution of an atom by a methyl group. Methylation is a form of alkylation, with a methyl group replacing a hydrogen atom. These terms are commonly used in chemistry, biochemistry, soil science, and biology. In biological systems, methylation is catalyzed by enzymes; such methylation can be involved in modification of heavy metals, regulation of gene expression, regulation of protein function, and RNA processing. In vitro methylation of tissue samples is also a way to reduce some histological staining artifacts. The reverse of methylation is demethylation.

text:
# Methylation

**Methylation**, in the chemical sciences, is the addition of a methyl group on a substrate, or the substitution of an atom (or group) by a methyl group. Methylation is a form of alkylation, with a methyl group replacing a hydrogen atom. These terms are commonly used in chemistry, biochemistry, soil science, and biology.

In biological systems, methylation is catalyzed by enzymes; such methylation can be involved in modification of heavy metals, regulation of gene expression, regulation of protein function, and RNA processing. *In vitro* methylation of tissue samples is also a way to reduce some histological staining artifacts. The reverse of methylation is demethylation.

## In biology

In biological systems, methylation is accomplished by enzymes. Methylation can modify heavy metals and can regulate gene expression, RNA processing, and protein function. It is a key process underlying epigenetics. Sources of methyl groups include S-methylmethionine, methyl folate, methyl B12.

### Methanogenesis

Methanogenesis, the process that generates methane from CO2, involves a series of methylation reactions. These reactions are caused by a set of enzymes harbored by a family of anaerobic microbes.

In reverse methanogenesis, methane is the methylating agent.

### O-methyltransferases

A wide variety of phenols undergo O-methylation to give anisole derivatives. This process, catalyzed by such enzymes as caffeoyl-CoA O-methyltransferase, is a key reaction in the biosynthesis of lignols, percursors to lignin, a major structural component of plants.

Plants produce flavonoids and isoflavones with methylations on hydroxyl groups, i.e. methoxy bonds. This 5-O-methylation affects the flavonoid's water solubility. Examples are 5-O-methylgenistein, 5-O-methylmyricetin, and 5-O-methylquercetin (azaleatin).

### Proteins

Along with ubiquitination and phosphorylation, methylation is a major biochemical process for modifying protein function. The most prevalent protein methylations affect arginine and lysine residue of specific histones. Otherwise histidine, glutamate, asparagine, cysteine are susceptible to methylation. Some of these products include *S*-methylcysteine, two isomers of *N*-methylhistidine, and two isomers of *N*-methylarginine.

#### Methionine synthase

Methionine synthase regenerates methionine (Met) from homocysteine (Hcy). The overall reaction transforms 5-methyltetrahydrofolate (N5-MeTHF) into tetrahydrofolate (THF) while transferring a methyl group to Hcy to form Met. Methionine Syntheses can be cobalamin-dependent and cobalamin-independent: Plants have both, animals depend on the methylcobalamin-dependent form.

In methylcobalamin-dependent forms of the enzyme, the reaction proceeds by two steps in a ping-pong reaction. The enzyme is initially primed into a reactive state by the transfer of a methyl group from N5-MeTHF to Co(I) in enzyme-bound cobalamin ((Cob), also known as vitamine B12)) , , forming methyl-cobalamin(Me-Cob) that now contains Me-Co(III) and activating the enzyme. Then, a Hcy that has coordinated to an enzyme-bound zinc to form a reactive thiolate reacts with the Me-Cob. The activated methyl group is transferred from Me-Cob to the Hcy thiolate, which regenerates Co(I) in Cob, and Met is released from the enzyme.

### Heavy metals: arsenic, mercury, cadmium

Biomethylation is the pathway for converting some heavy elements into more mobile or more lethal derivatives that can enter the food chain. The biomethylation of arsenic compounds starts with the formation of methanearsonates. Thus, trivalent inorganic arsenic compounds are methylated to give methanearsonate. S-adenosylmethionine is the methyl donor. The methanearsonates are the precursors to dimethylarsonates, again by the cycle of reduction (to methylarsonous acid) followed by a second methylation. Related pathways are found in the microbial methylation of mercury to methylmercury.

### Epigenetic methylation

#### DNA methylation

DNA methylation is the conversion of the cytosine to 5-methylcytosine. The formation of Me-CpG is catalyzed by the enzyme DNA methyltransferase. In vertebrates, DNA methylation typically occurs at CpG sites (cytosine-phosphate-guanine sites—that is, sites where a cytosine is directly followed by a guanine in the DNA sequence). In mammals, DNA methylation is common in body cells, and methylation of CpG sites seems to be the default. Human DNA has about 80–90% of CpG sites methylated, but there are certain areas, known as CpG islands, that are CG-rich (high cytosine and guanine content, made up of about 65% CG residues), wherein none is methylated. These are associated with the promoters of 56% of mammalian genes, including all ubiquitously expressed genes. One to two percent of the human genome are CpG clusters, and there is an inverse relationship between CpG methylation and transcriptional activity. Methylation contributing to epigenetic inheritance can occur through either DNA methylation or protein methylation. Improper methylations of human genes can lead to disease development, including cancer.

In honey bees, DNA methylation is associated with alternative splicing and gene regulation based on functional genomic research published in 2013. In addition, DNA methylation is associated with expression changes in immune genes when honey bees were under lethal viral infection. Several review papers have been published on the topics of DNA methylation in social insects.

#### RNA methylation

**RNA methylation** occurs in different RNA species viz. tRNA, rRNA, mRNA, tmRNA, snRNA, snoRNA, miRNA, and viral RNA. Different catalytic strategies are employed for RNA methylation by a variety of RNA-methyltransferases. RNA methylation is thought to have existed before DNA methylation in the early forms of life evolving on earth.

N6-methyladenosine (m6A) is the most common and abundant methylation modification in RNA molecules (mRNA) present in eukaryotes. 5-methylcytosine (5-mC) also commonly occurs in various RNA molecules. Recent data strongly suggest that m6A and 5-mC RNA methylation affects the regulation of various biological processes such as RNA stability and mRNA translation, and that abnormal RNA methylation contributes to etiology of human diseases.

In social insects such as honey bees, RNA methylation is studied as a possible epigenetic mechanism underlying aggression via reciprocal crosses.

#### Protein methylation

Protein methylation typically takes place on arginine or lysine amino acid residues in the protein sequence. Arginine can be methylated once (monomethylated arginine) or twice, with either both methyl groups on one terminal nitrogen (asymmetric dimethylarginine) or one on both nitrogens (symmetric dimethylarginine), by protein arginine methyltransferases (PRMTs). Lysine can be methylated once, twice, or three times by lysine methyltransferases. Protein methylation has been most studied in the histones. The transfer of methyl groups from S-adenosyl methionine to histones is catalyzed by enzymes known as histone methyltransferases. Histones that are methylated on certain residues can act epigenetically to repress or activate gene expression. Protein methylation is one type of post-translational modification.

### Evolution

Methyl metabolism is very ancient and can be found in all organisms on earth, from bacteria to humans, indicating the importance of methyl metabolism for physiology. Indeed, pharmacological inhibition of global methylation in species ranging from human, mouse, fish, fly, roundworm, plant, algae, and cyanobacteria causes the same effects on their biological rhythms, demonstrating conserved physiological roles of methylation during evolution.

## In chemistry

The term methylation in organic chemistry refers to the alkylation process used to describe the delivery of a CH3 group.

### Electrophilic methylation

Methylations are commonly performed using *electrophilic* methyl sources such as iodomethane, dimethyl sulfate, dimethyl carbonate, or tetramethylammonium chloride. Less common but more powerful (and more dangerous) methylating reagents include methyl triflate, diazomethane, and methyl fluorosulfonate (magic methyl). These reagents all react via SN2 nucleophilic substitutions. For example, a carboxylate may be methylated on oxygen to give a methyl ester; an alkoxide salt RO may be likewise methylated to give an ether, ROCH3; or a ketone enolate may be methylated on carbon to produce a new ketone.

The Purdie methylation is a specific for the methylation at oxygen of carbohydrates using iodomethane and silver oxide.

### Eschweiler–Clarke methylation

The Eschweiler–Clarke reaction is a method for methylation of amines. This method avoids the risk of quaternization, which occurs when amines are methylated with methyl halides.

### Diazomethane and trimethylsilyldiazomethane

Diazomethane and the safer analogue trimethylsilyldiazomethane methylate carboxylic acids, phenols, and even alcohols:

$$\ce {RCO2H + tmsCHN2 + CH3OH -\> RCO2CH3 + CH3Otms + N2}$$

The method offers the advantage that the side products are easily removed from the product mixture.

### Nucleophilic methylation

Methylation sometimes involve use of *nucleophilic* methyl reagents. Strongly nucleophilic methylating agents include methyllithium (CH3Li) or Grignard reagents such as methylmagnesium bromide (CH3MgX). For example, CH3Li will add methyl groups to the carbonyl (C=O) of ketones and aldehyde.:

Milder methylating agents include tetramethyltin, dimethylzinc, and trimethylaluminium.

### Biology topics

### Organic chemistry topics

* deltaMasses Detection of Methylations after Mass Spectrometry


title: WKGR

abstract: WKGR is a mainstream rock station licensed to Wellington, Florida and serving the West Palm Beach market. Owned by iHeartMedia, Inc., it transmits at 100,000 watts effective radiated power with an antenna height above average terrain of 299 meters. WKGR's signal can be picked up as far north as Melbourne, as far west as Moore Haven, and usually no further south than Interstate 595 in Fort Lauderdale. Its transmitter is located on the west side of Jonathan Dickinson State Park in Hobe Sound. Also sharing WKGR's transmitter tower are stations WIRK and WMBX. WKGR previously simulcast the programming of sister station WJNO on its HD2 subchannel starting in September 2010; by 2013 this was replaced with the signal of Christian rock station WREH. WKGR later went to classic country on HD2, and in 2019, dropped its HD2 subchannel. Then on January 19, 2021, WKGR brought back its HD2 subchannel with its original programming, simulcasting WJNO. A few weeks later, sister station WBZT began simulcasting on its HD2 subchannel, with WJNO moving to the HD2 subchannel of sister station WLDI. As of December 2023, the WJNO simulcast returned to the HD2 subchannel.

text:
# WKGR

**WKGR** (98.7 FM) is a mainstream rock station licensed to Wellington, Florida and serving the West Palm Beach market. Owned by iHeartMedia, Inc., it transmits at 100,000 watts effective radiated power with an antenna height above average terrain of 299 meters (981 feet). WKGR's signal can be picked up as far north as Melbourne, as far west as Moore Haven, and usually no further south than Interstate 595 in Fort Lauderdale. Its transmitter is located on the west side of Jonathan Dickinson State Park in Hobe Sound. Also sharing WKGR's transmitter tower are stations WIRK (which itself was a primary competitor of WKGR before moving its rock programming to an HD Radio subchannel) and WMBX.

WKGR previously simulcast the programming of sister station WJNO on its HD2 subchannel starting in September 2010; by 2013 this was replaced with the signal of Christian rock station WREH. WKGR later went to classic country on HD2, and in 2019, dropped its HD2 subchannel. Then on January 19, 2021, WKGR brought back its HD2 subchannel with its original programming, simulcasting WJNO. A few weeks later, sister station WBZT began simulcasting on its HD2 subchannel, with WJNO moving to the HD2 subchannel of sister station WLDI. As of December 2023, the WJNO simulcast returned to the HD2 subchannel.

27°01′32″N 80°10′42″W / 27.025611°N 80.178389°W / 27.025611; -80.178389

1. "Facility Technical Data for WKGR". *Licensing and Management System*. Federal Communications Commission.

## InfoBox

WKGR
|  | |
| --- | --- |
| Broadcast area | Palm BeachPort St. Lucie, Florida |
| Frequency | 98.7 MHz (HD Radio) |
| Branding | 98.7 The Gator |
| Programming | |
| Language(s) | English |
| Format | Mainstream rock |
| Subchannels | HD2: WJNO simulcast (News/talk) |
| Ownership | |
| Owner |  |
| Sister stations | WAVW, WBZT, WCZR, WJNO, WLDI, WOLL, WQOL, WZTA, WZZR |
| History | |
| First air date | 1961 (1961) |
| Former call signs | * WLQY (1961–1980) * WIZD (1980–1984) |
| Call sign meaning | WK Gater |
| Technical information | |
| Licensing authority | FCC |
| Facility ID | 1245 |
| Class | C1 |
| ERP | 100,000 watts |
| HAAT | 299 m (981 ft) |
| Links | |
| Public license information |  |
| Webcast | Listen live (via iHeartRadio) |
| Website | gaterrocks.iheart.com |


title: 1979 Currie Cup

abstract: The 1979 Currie Cup was the 41st edition of the Currie Cup, the premier annual domestic rugby union competition in South Africa. The tournament was jointly won by Northern Transvaal and Western Province after the two teams drew 15–15 in the final in Cape Town.

text:
# 1979 Currie Cup

The **1979 Currie Cup** was the 41st edition of the Currie Cup, the premier annual domestic rugby union competition in South Africa.

The tournament was jointly won by Northern Transvaal (for the 11th time) and Western Province (for the 22nd time) after the two teams drew 15–15 in the final in Cape Town.

## Results

### Semi-finals

|  |  | Eastern Province | 6–16 | Northern Transvaal | Boet Erasmus Stadium, Port Elizabeth |  |
| --- | --- | --- | --- | --- | --- | --- |
| |  |  |  | Report |  |  |

|  |  | Griqualand West | 15–20 | Western Province | De Beers Stadium, Kimberley |  |
| --- | --- | --- | --- | --- | --- | --- |
| |  |  |  | Report |  |  |

### Final

|  |  | Western Province | 15–15 | Northern Transvaal | Newlands Stadium, Cape Town |  |
| --- | --- | --- | --- | --- | --- | --- |
| |  |  |  | Report |  | Referee: Steve Strydom |

## InfoBox

| 1979 Currie Cup | |
| --- | --- |
| Countries | South Africa |
| Champions | Joint winners:
Northern Transvaal (11th title)
Western Province (22nd title) |
|  | |


title: Provimi

abstract: Provimi is a company specializing in animal nutrition and related products. In the 1930s it started selling a product under the name Provimi, a mixture of three basic elements in every animal feed and this is where the present name is derived from: Proteins, Vitamins and Minerals. The company is of Dutch origin and headquartered in Rotterdam.

text:
# Provimi

**Provimi** is a company specializing in animal nutrition and related products. In the 1930s it started selling a product under the name Provimi, a mixture of three basic elements in every animal feed and this is where the present name is derived from: Proteins, Vitamins and Minerals. The company is of Dutch origin and headquartered in Rotterdam.

## History

Provimi was founded near Rotterdam, the Netherlands in 1927, where it started up as a trading company for Dutch farmers.

In 1971, the American agricultural company Central Soya bought Provimi. In 1988, Central Soya was taken over by Eridania Béghin-Say Group, a large French agribusiness conglomerate. In the years to follow, Provimi went through a period of internal and worldwide external expansion until 2001, when the Eridania Béghin-Say Group was broken into four companies, one of which was Provimi.

In 2002, Provimlux, a holding company jointly controlled by funds advised by CVC Capital Partners and PAI Partners, acquired the 53.66% majority shareholding of Provimi. After the subsequent execution of a standing offer, Provimlux held 74.05% of Provimi, which remained listed on Euronext. In the years to follow, Provimi continued its external growth.

In April 2007, Permira bought the majority of Provimi's shares from CVC Capital Partners and PAI Partners. The Provimi Group was delisted from the Euronext Stock Exchange in Paris on 6 November 2009 and is wholly owned by KoroFrance SAS, a company indirectly controlled by investment funds managed or advised by Permira Advisers LLP.

In November 2011 the company was acquired by Cargill for €1.5 billion ($2.1 billion US).

* Group's Review Provimi, June 2007


title: Thomas Kirby House

abstract: The Thomas Kirby House in Kendrick, Idaho was built in 1889 and modified in 1910 and otherwise. It was built for Thomas Kirby, a man highly responsible for the railroads that started in Kendrick and went to Troy, Idaho. The house is eclectic Queen Anne in style, with elements of Stick and Eastlake architecture. The 1998 NRHP nomination stated it "still commands attention and is significant as one of the best remaining examples of Victorian residential architecture in Idaho's North-Central region." It was listed on the National Register of Historic Places in 1999.

text:
# Thomas Kirby House

The **Thomas Kirby House** in Kendrick, Idaho was built in 1889 and modified in 1910 and otherwise. It was built for Thomas Kirby, a man highly responsible for the railroads that started in Kendrick and went to Troy, Idaho.

The house is eclectic Queen Anne in style, with elements of Stick and Eastlake architecture. The 1998 NRHP nomination stated it "still commands attention and is significant as one of the best remaining examples of Victorian residential architecture in Idaho's North-Central region."

It was listed on the National Register of Historic Places in 1999.

## InfoBox

|  | |
| --- | --- |
| Thomas Kirby House | |
| U.S. National Register of Historic Places | |
|  | |
|  | |
|  | |
| Location | 102 N. 9th St., Kendrick, Idaho |
| Coordinates | 46°36′51″N 116°38′49″W / 46.614164°N 116.646829°W / 46.614164; -116.646829 |
| Area | less than one acre |
| Built | 1889 |
| Architectural style | Queen Anne |
| NRHP reference No. | 99000414 |
| Added to NRHP | April 1, 1999 |


title: Pasturka

abstract: Pasturka is a village in the administrative district of Gmina Pińczów, within Pińczów County, Świętokrzyskie Voivodeship, in south-central Poland. It lies approximately 5 kilometres (3 mi) south-east of Pińczów and 44 km (27 mi) south of the regional capital Kielce.

text:
# Pasturka

**Pasturka** \[pasˈturka\] is a village in the administrative district of Gmina Pińczów, within Pińczów County, Świętokrzyskie Voivodeship, in south-central Poland. It lies approximately 5 kilometres (3 mi) south-east of Pińczów and 44 km (27 mi) south of the regional capital Kielce.

## InfoBox

| Pasturka | |
| --- | --- |
| Village | |
| Pasturka | |
| Coordinates: 50°29′50″N 20°33′42″E / 50.49722°N 20.56167°E / 50.49722; 20.56167 | |
| Country | Poland |
| Voivodeship | Świętokrzyskie |
| County | Pińczów |
| Gmina | Pińczów |
| Population(approx.) | 360 |


title: Presbyornis

abstract: Presbyornis is an extinct genus of presbyornithid bird from North America during the Paleogene period, between the Late Paleocene and Early Eocene.

text:
# Presbyornis

***Presbyornis*** is an extinct genus of presbyornithid bird from North America during the Paleogene period, between the Late Paleocene and Early Eocene.

## History of discovery

The fossil record of *P. pervetus* includes many complete skeletons from Green River Formation sites (Early Eocene), suggesting that the birds nested in colonies and that they possibly died due to volcanism or botulism, the latter of which is similar to many colony-nesting waterfowl or shorebirds today. Fossils identified as *P.* cf. *pervetus* have been discovered from the Margaret Formation of Ellesmere Island, where the remains of *Gastornis* sp. have also been found.

*P. recurvirostra* is known from a partial wing (KUVP 10105) found in the Colton Formation, from the Late Paleocene to Early Eocene sediments of the Wasatch Plateau near Ephraim, Utah. *P. isoni*, much larger than *P. pervetus*, is known from the Late Paleocene Aquia Formation in Maryland, based on the partial humerus (USNM 294116) and partial fingerbone (USNM 294117) that were initially described, as well as a complete humerus (SMM P96.9.2). Three humeri that were initially believed to be from *Headonornis* are suggested to belong to *P. isoni*, and the holotype coracoid of *Headonornis* may also be assigned to as *P. isoni*, though these claims require additional material for confirmation. However, *Headonornis* is now referred to as a stem group representative of the Phoenicopteriformes.

The holotype and paratypes of "*P.*" *mongoliensis* are known from the Early Eocene of Mongolia, but these fragmentary specimens are poorly preserved and they likely belong to a stem Phoenicopterimorphae, not a presbyornithid. Undescribed fossils are also known from the Paleocene of Utah. *Wunketru howardae*, previously thought to be a species of *Telmabates* or a junior synonym of *P. pervetus*, is now considered a distinct anseriform.

## Description

Along with *Teviornis*, *Presbyornis* was one of the earliest stem anseriforms. Because of its long legs and neck, *Presbyornis* could stand up to 1 metre (3.3 ft) tall and was initially mistaken for a flamingo, but it was reclassified as an anseriform when the duck-like anatomy of its skull and bill was found. Later, it was believed to represent a transitional stage between the anseriforms and the shorebirds, but it is now considered a member of an extinct group of anseriforms which was most closely related to modern screamers. Judging from numerous fossil findings, *Presbyornis* is presumed to have lived in colonies around shallow lakes. Its broad, flat bill was used to filter food (small plants and animals) from the water, in the manner of today's dabbling ducks.

1. Hardy, J.W. (1959). "A Previously Undescribed Recurvirostrid from the Eocene of Utah". *The Auk*. **76** (1): 106–108. doi:10.2307/4081861. JSTOR 4081861.
2. Ericson, Per G.P. (2000-09-25). "Systematic revision, skeletal anatomy, and paleoecology of the New World early Tertiary Presbyornithidae (Aves: Anseriformes)" (PDF). *PaleoBios*. **20** (2): 1–23.
3. Kurochkin, E. N.; Dyke, G. J.; Karhu, A. A. (2002). "A new presbyornithid bird (Aves, Anseriformes) from the late Cretaceous of southern Mongolia". *American Museum Novitates* (3386): 1–11. doi:10.1206/0003-0082(2002)386\<0001:ANPBAA\>2.0.CO;2. hdl:2246/2875. S2CID 59147935.
4. Kurochkin, Evgeney N.; Dyke, Gareth J. (2010). "A Large Collection of *Presbyornis* (Aves, Anseriformes, Presbyornithidae) from the Late Paleocene and Early Eocene of Mongolia". *Geological Journal*. **45** (4): 375–387. Bibcode:2010GeolJ..45..375K. doi:10.1002/gj.1177. S2CID 140588679.
5. Jobling, James A. (2010). *The Helm Dictionary of Scientific Bird Names*. London: Christopher Helm. p. 331. ISBN 978-1-4081-2501-4.
6. "Article 31. Species-group names". Retrieved May 29, 2024. A species-group name that is a simple or compound noun (or noun phrase) in apposition need not agree in gender with the generic name with which it is combined (the original spelling is to be retained, with gender ending unchanged; see Article 34.2.1).
7. De Pietri, V.L.; Scofield, R.P.; Zelenkov, N.; Boles, W.E.; Worthy, T.H. (2016). "The unexpected survival of an ancient lineage of anseriform birds into the Neogene of Australia: the youngest record of Presbyornithidae". *Royal Society Open Science*. **3** (2): 150635. Bibcode:2016RSOS....350635D. doi:10.1098/rsos.150635. PMC 4785986. PMID 26998335.
8. Worthy, Trevor H.; De Pietri, Vanesa L.; Scofield, R. Paul; Hand, Suzanne J. (2023-03-20). "A new Eocene species of presbyornithid (Aves, Anseriformes) from Murgon, Australia". *Alcheringa: An Australasian Journal of Palaeontology*. **47** (4): 416–430. Bibcode:2023Alch...47..416W. doi:10.1080/03115518.2023.2184491. ISSN 0311-5518. S2CID 257679005.
9. Zelenkov, N. V. (2021). "A revision of the Palaeocene–Eocene Mongolian Presbyornithidae (Aves: Anseriformes)". *Paleontological Journal*. **55** (3). doi:10.31857/S0031031X21030132.
10. Stidham, Thomas A.; Eberle, Jaelyn J. (2016). "The palaeobiology of high latitude birds from the early Eocene greenhouse of Ellesmere Island, Arctic Canada". *Scientific Reports*. **6**: Article number 20912. Bibcode:2016NatSR...620912S. doi:10.1038/srep20912. PMC 4751439. PMID 26867798.
11. Olson, S. (1994). "A giant *Presbyornis* (Aves: Anseriformes) and other birds from the Paleocene Aquia Formation of Maryland and Virginia". *Proceedings of the Biological Society of Washington*. **107**: 429–435. hdl:10088/6493.
12. Dyke, Gareth J. (2001). "The fossil waterfowl (Aves: Anseriformes) from the Eocene of England". *American Museum Novitates* (3354): 1–15. doi:10.1206/0003-0082(2001)354\<0001:TFWAAF\>2.0.CO;2.
13. Mayr, G. (2009). "Phoenicopteriformes (flamingos) and Podicipediformes (grebes)". *Paleogene Fossil Birds*. Springer. pp. 105–109. doi:10.1007/978-3-540-89628-9\_10. ISBN 978-3-540-89628-9.
14. De Mendoza, Ricardo Santiago; Degrange, Federico Javier; Tambussi, Claudia Patricia (2024). "An assessment of the anseriform affinities of *"Telmabates" howardae*". *Journal of South American Earth Sciences*. **135**. 104786. Bibcode:2024JSAES.13504786D. doi:10.1016/j.jsames.2024.104786. S2CID 267159455.
15. Palmer, D., ed. (1999). *The Marshall Illustrated Encyclopedia of Dinosaurs and Prehistoric Animals*. London: Marshall Editions. p. 181. ISBN 1-84028-152-9.

## References

* Dyke, Gareth J. (2001): The Fossil Waterfowl (Aves: Anseriformes) from the Eocene of England. *American Museum Novitates* **3354**: 1–15. PDF fulltext
* Palmer, D., ed. (1999). *The Marshall Illustrated Encyclopedia of Dinosaurs and Prehistoric Animals*. London: Marshall Editions. p. 181. ISBN 1-84028-152-9.
* Wetmore, Alexander (1926): Fossil birds from the Green River Deposits of Eastern Utah. *Annals of the Carnegie Museum* **16**: 391–402.

## InfoBox

| *Presbyornis*
Temporal range: | |
| --- | --- |
|  | |
| An assemblage of *Presbyornis pervetus* skeletons (AMNH 28505) | |
|
| Scientific classification | |
| Domain: | Eukaryota |
| Kingdom: | Animalia |
| Phylum: | Chordata |
| Class: | Aves |
| Family: | Presbyornithidae |
| Genus: | *Presbyornis*
Wetmore, 1926 |
|
| Species | |
| * *P. pervetus* Wetmore, 1926 (type) * *P. recurvirostra* (Hardy, 1959) * *P. isoni* Olson, 1994 * "*P.*" *mongoliensis* Kurochkin & Dyke, 2010 | |
| Synonyms | |
|  | |


title: Malik Ahmad Yar Hunjra

abstract: Malik Ahmad Yar Hunjra is a Pakistani politician who was a Member of the Provincial Assembly of the Punjab, from 2002 to May 2018.

text:
# Malik Ahmad Yar Hunjra

**Malik Ahmad Yar Hunjra** (born on 6th March 1960) is a Pakistani politician who was a Member of the Provincial Assembly of the Punjab, from 2002 to May 2018.

## Early life and education

He was born on 6 March 1978 in Muzaffargarh District.

He graduated from Government College University where he was enrolled between 1997 and 2000. He obtained the degree of Master of Business Administration in Finance from Quaid-i-Azam University in 2003 and graduated in Law from Bahauddin Zakariya University. He has the degree of Bachelor of Laws. He belongs to a political family of South Punjab whose head is Sultan Mehmood Hunjra

## Political career

He was elected to the Provincial Assembly of the Punjab as a candidate of Pakistan Muslim League (Q) (PML-Q) from Constituency PP-251 (Muzaffargarh-I) in 2002 Pakistani general election. He received 21,695 votes and defeated Mufti Abdul Jalil, a candidate of Muttahida Majlis-e-Amal (MMA). In the same election, he ran for the seat of the National Assembly of Pakistan as an independent candidate from Constituency NA-176 (Muzaffargarh-I) but was unsuccessful. He received 2,823 votes and lost the seat to Khalida Mohsin Ali Qureshi, a candidate of Pakistan Peoples Party (PPP).

He was re-elected to the Provincial Assembly of the Punjab as a candidate of PML-Q from Constituency PP-251 (Muzaffargarh-I) in 2008 Pakistani general election. He received 19,913 votes and defeated Malik Muhammad Yousaf Hinjra, a candidate of PPP.

He was re-elected to the Provincial Assembly of the Punjab as a candidate of Pakistan Muslim League (N) from Constituency PP-251 (Muzaffargarh-I) in 2013 Pakistani general election. He received 33,502 votes and defeated Muhammad Ashraf Khan Rind, a candidate of Pakistan Tehreek-e-Insaf (PTI). In November 2016, he was inducted into the provincial Punjab cabinet of Chief Minister Shehbaz Sharif and was made Provincial Minister of Punjab for Prisons.

## InfoBox

| Malik Ahmad Yar Hunjra | |
| --- | --- |
| ملک احمد یار ہنجرا | |
|  | |
| Member of the Provincial Assembly of the Punjab | |
| **In office**
2002  31 May 2018 | |
|  | |
| Personal details | |
| Born | (1960-03-06) 6 March 1960
Muzaffargarh District |
| Nationality | Pakistani |
| Political party | Pakistan Muslim League (Nawaz) |
| Relations | Malik Ghulam Qasim Hanjra (brother)
Sultan Mehmood Hanjra (uncle) |
|  | |


title: Triumph Tigress/BSA Sunbeam

abstract: The Triumph Tigress, also sold as the BSA Sunbeam, was a scooter designed to have good performance and handling for the motorcycle enthusiast. The entry of the BSA group into the scooter field was announced by Edward Turner in October 1958. The 250 cc model would have a cruising speed of 55 to 60 mph and petrol consumption of 120 miles per imperial gallon. A prototype 250 cc BSA Sunbeam was displayed at the 1958 Earl's Court Cycle and Motor Cycle Show. Manufacture started in late 1959, but delivery difficulties were acknowledged due to problems with recruiting labour, although it was claimed that the group had a manufacturing capacity of 50,000 machines a year. The design by Edward Turner drew on Triumph's long experience of building fast motorcycles, and was sold under two brand names to take advantage of established distribution networks. This badge engineering was one of the last uses of the Sunbeam marque. The differences between the BSA Sunbeam and Triumph Tigress were entirely cosmetic - the former in polychromatic green paint, also two-tone red and cream, with a BSA badge; the latter in a shell blue or mimosa and ivory with Triumph badging. The scooter was available with a 250 cc four-stroke twin or 175 cc two-stroke single-cylinder engine. Both engines were forced-air-cooled and curbed to keep low petrol consumption. The two-stroke was a development of the BSA Bantam engine but the four-stroke was a completely new parallel-twin with gear rather than chain drive to the gearbox. The contact-breaker fed two ignition coils, each of which had a lead to its spark plug without a distributor. Drive to the rear wheel was by a fully enclosed chain in an oil bath. Both versions had four, foot-operated gears. Some of the 250 twins were fitted with an electric starter and a 12 volt electrical system. The 250 twin sold well and could do 70 mph (113 km/h) with efficient suspension and good roadholding despite having only 10-inch wheels. The weight was low in comparison to other scooters. The only problem was build quality: it was sometimes said that a Tigress was a joy to own so long as someone else was paying the repair bills. The 250 cc four-stroke model was discontinued in 1964, the 175 cc two-stroke model in 1965. Later in the 1960s, despite internal opposition from those who felt that scooters would dilute the macho image of the brand, Triumph produced another scooter and a motor tricycle for "shoppers". The Triumph Tina and the Ariel 3 tricycle were intended to tap into the market segment for a convenient 'shopping basket'.

text:
# Triumph Tigress/BSA Sunbeam

The **Triumph Tigress**, also sold as the **BSA Sunbeam**, was a scooter designed to have good performance and handling for the motorcycle enthusiast. The entry of the BSA group into the scooter field was announced by Edward Turner in October 1958. The 250 cc model would have a cruising speed of 55 to 60 mph (89 to 97 km/h) and petrol consumption of 120 miles per imperial gallon (2.4 L/100 km; 100 mpgUS). A prototype 250 cc BSA Sunbeam was displayed at the 1958 Earl's Court Cycle and Motor Cycle Show. Manufacture started in late 1959, but delivery difficulties were acknowledged due to problems with recruiting labour, although it was claimed that the group had a manufacturing capacity of 50,000 machines a year.

The design by Edward Turner drew on Triumph's long experience of building fast motorcycles, and was sold under two brand names to take advantage of established distribution networks. This badge engineering was one of the last uses of the Sunbeam marque. The differences between the BSA Sunbeam and Triumph Tigress were entirely cosmetic - the former in polychromatic green paint, also two-tone red and cream, with a BSA badge; the latter in a shell blue or mimosa and ivory (two tone) with Triumph badging.

The scooter was available with a 250 cc four-stroke twin (10 hp; 7.5 kW) or 175 cc two-stroke single-cylinder engine (7.5 hp; 5.6 kW). Both engines were forced-air-cooled and curbed to keep low petrol consumption. The two-stroke was a development of the BSA Bantam engine but the four-stroke was a completely new parallel-twin with gear rather than chain drive to the gearbox. The contact-breaker fed two ignition coils, each of which had a lead to its spark plug without a distributor. Drive to the rear wheel was by a fully enclosed chain in an oil bath. Both versions had four, foot-operated gears. Some of the 250 twins were fitted with an electric starter and a 12 volt (not 6 volt) electrical system. The 250 twin sold well and could do 70 mph (113 km/h) with efficient suspension and good roadholding despite having only 10-inch wheels. The weight was low in comparison to other scooters (100/110 kg). The only problem was build quality: it was sometimes said that a *Tigress* was a joy to own so long as someone else was paying the repair bills.

The 250 cc four-stroke model was discontinued in 1964, the 175 cc two-stroke model in 1965.

Later in the 1960s, despite internal opposition from those who felt that scooters would dilute the macho image of the brand, Triumph (owned by BSA) produced another scooter and a motor tricycle for "shoppers". The Triumph Tina and the Ariel 3 tricycle (BSA also owned the Ariel marque) were intended to tap into the market segment for a convenient 'shopping basket'.


title: Love no Theme

abstract: Love no Teema "Love no Theme" is Ai Otsuka's first single under the avex trax label under her pen name Love. It is also her second single released in 2007. "Love no Theme", marks the first time that Ai has released a single about a character bunny name Love-chan and under her pen name Love. "I canChu♥" was the original title but it was changed to "Love no Theme". "Love no Theme" also the opening theme for the Oshare Majo: Love and Berry anime movie, Oshare Majo: Love and Berry Shiwase no Mahou.

text:
# Love no Theme

"**Love no Theme**" is Ai Otsuka's first (15th overall) single under the avex trax label under her pen name Love. It is also her second single released in 2007.

"Love no Theme", marks the first time that Ai has released a single about a character bunny name Love-chan and under her pen name Love. "I canChu♥" was the original title but it was changed to "Love no Theme".

"Love no Theme" also the opening theme for the **Oshare Majo: Love and Berry** anime movie, Oshare Majo: Love and Berry Shiwase no Mahou.

## Track listing

### CD

1. Love no Teema (LOVE's Theme , LOVEのテーマ)
2. Love no Teema (instrumental)
3. Next Single Preview (White Choco)

### DVD

1. Love no Theme (PV)

## Charts

Oricon Sales Chart (Japan)

| Chart | Peak Position | First Week Sales | Sales Total | Chart Run |
| --- | --- | --- | --- | --- |
| Oricon Daily Charts | #9 |  | N/A |  |
| Oricon Weekly Charts | #22 | 4,790 | 8,537 | 5 |
| Oricon Monthly Charts |  |  |  |  |
| Oricon Yearly Charts |  |  |  |  |
|

## InfoBox

| "Loveのテーマ"
"LOVE no Theme" / "Love's Theme" | |
| --- | --- |
|  | |
| Single by Love | |
| Released | April 11, 2007 |
| Recorded | 2007 |
| Genre | J-Pop |
| Label | avex trax
AVCD-31230/B (Japan, CD+DVD)
AVCD-31231 (Japan, CD) |
| Songwriter(s) | Ai Otsuka |
| Love singles chronology | |
| "**Loveのテーマ"
"LOVE no Theme" / "Love's Theme**"
(2007) "White Choco"
(2007) | |
|  | |
| Ai Otsuka singles chronology | |
| "Chu-Lip"
(2007)  "Peach / Heart"
(2007) | |
| Alternative cover | |
|  | |
| The CD + DVD Cover | |
|  | |
|  | |


title: Methylated DNA immunoprecipitation

abstract: Methylated DNA immunoprecipitation is a large-scale purification technique in molecular biology that is used to enrich for methylated DNA sequences. It consists of isolating methylated DNA fragments via an antibody raised against 5-methylcytosine (5mC). This technique was first described by Weber M. et al. in 2005 and has helped pave the way for viable methylome-level assessment efforts, as the purified fraction of methylated DNA can be input to high-throughput DNA detection methods such as high-resolution DNA microarrays (MeDIP-chip) or next-generation sequencing (MeDIP-seq). Nonetheless, understanding of the methylome remains rudimentary; its study is complicated by the fact that, like other epigenetic properties, patterns vary from cell-type to cell-type.

text:
# Methylated DNA immunoprecipitation

**Methylated DNA immunoprecipitation** (MeDIP or mDIP) is a large-scale (chromosome\- or genome-wide) purification technique in molecular biology that is used to enrich for methylated DNA sequences. It consists of isolating methylated DNA fragments via an antibody raised against 5-methylcytosine (5mC). This technique was first described by Weber M. *et al.* in 2005 and has helped pave the way for viable methylome-level assessment efforts, as the purified fraction of methylated DNA can be input to high-throughput DNA detection methods such as high-resolution DNA microarrays (MeDIP-chip) or next-generation sequencing (MeDIP-seq). Nonetheless, understanding of the methylome remains rudimentary; its study is complicated by the fact that, like other epigenetic properties, patterns vary from cell-type to cell-type.

## Background

DNA methylation, referring to the reversible methylation of the 5 position of cytosine by methyltransferases, is a major epigenetic modification in multicellular organisms. In mammals, this modification primarily occurs at CpG sites, which in turn tend to cluster in regions called CpG islands. There is a small fraction of CpG islands that can overlap or be in close proximity to promoter regions of transcription start sites. The modification may also occur at other sites, but methylation at either of these sites can repress gene expression by either interfering with the binding of transcription factors or modifying chromatin structure to a repressive state.

Disease condition studies have largely fueled the effort in understanding the role of DNA methylation. Currently, the major research interest lies in investigating disease conditions such as cancer to identify regions of the DNA that has undergone extensive methylation changes. The genes contained in these regions are of functional interest as they may offer a mechanistic explanation to the underlying genetic causes of a disease. For instance, the abnormal methylation pattern of cancer cells was initially shown to be a mechanism through which tumor suppressor-like genes are silenced, although it was later observed that a much broader range of gene types are affected.

### Other technologies

There are two approaches to methylation analysis: typing and profiling technologies. Typing technologies are targeted towards a small number of loci across many samples, and involve the use of techniques such as PCR, restriction enzymes, and mass spectrometry. Profiling technologies such as MeDIP are targeted towards a genome\- or methylome-wide level assessment of methylation; this includes restriction landmark genomic scanning (RLGS), and bisulfite conversion-based methods, which rely on the treatment of DNA with bisulfite to convert unmethylated cytosine residues to uracil.

### Limitations of other technologies

Other methods mapping and profiling the methylome have been effective but are not without their limitations that can affect resolution, level of throughput, or experimental variations. For instance, RLGS is limited by the number of restriction sites in genome that can be targets for the restriction enzyme; typically, a maximum of ~4100 landmarks can be assessed. Bisulfite sequencing-based methods, despite possible single-nucleotide resolution, have a drawback: the conversion of unmethylated cytosine to uracil can be unstable. In addition, when bisulfite conversion is coupled with DNA microarrays to detect bisulfite converted sites, the reduced sequence complexity of DNA is a problem. Microarrays capable of comprehensively profiling the whole-genome become difficult to design as fewer unique probes are available.

## Methods

The following sections outline the method of MeDIP coupled with either high-resolution array hybridization or high-throughput sequencing. Each DNA detection method will also briefly describe post-laboratory processing and analysis. Different post-processing of the raw data is required depending on the technology used to identify the methylated sequences. This is analogous to data generated using ChIP-chip and ChIP-seq.

### Methylated DNA immunoprecipitation (MeDIP)

Genomic DNA is extracted (DNA extraction) from the cells and purified. The purified DNA is then subjected to sonication to shear it into random fragments. This sonication process is quick, simple, and avoids restriction enzyme biases. The resulting fragments range from 300 to 1000 base pairs (bp) in length, although they are typically between 400 and 600 bp. The short length of these fragments is important in obtaining adequate resolution, improving the efficiency of the downstream step in immunoprecipitation, and reducing fragment-length effects or biases. Also, the size of the fragment affects the binding of 5-methyl-cytidine (5mC) antibody because the antibody needs more than just a single 5mC for efficient binding. To further improve binding affinity of the antibodies, the DNA fragments are denatured to produce single-stranded DNA. Following denaturation, the DNA is incubated with monoclonal 5mC antibodies. The classical immunoprecipitation technique is then applied: magnetic beads conjugated to anti-mouse-IgG are used to bind the anti-5mC antibodies, and unbound DNA is removed in the supernatant. To purify the DNA, proteinase K is added to digest the antibodies and release the DNA, which can be collected and prepared for DNA detection.

For more details regarding the experimental steps see.

### MeDIP and array-based hybridization (MeDIP-chip)

A fraction of the input DNA obtained after the sonication step above is labeled with cyanine-5 (Cy5; red) deoxy-cytosine-triphosphate while the methylated DNA, enriched after the immunoprecipitation step, is labeled with cyanine-3 (Cy3; green). The labeled DNA samples are cohybridized on a 2-channel, high-density genomic microarray to probe for presence and relative quantities. The purpose of this comparison is to identify sequences that show significant differences in hybridization levels, thereby confirming the sequence of interest is enriched. Array-based identification of MeDIP sequences are limited to the array design. As a result, the resolution is restricted to the probes in the array design. There are additional standard steps required in signal processing to correct for hybridization issues such as noise, as is the case with most array technologies.

See for more details.

### MeDIP and high-throughput sequencing (MeDIP-seq)

The MeDIP-seq approach, i.e. the coupling of MeDIP with next generation, short-read sequencing technologies such as 454 pyrosequencing or Illumina (Solexa), was first described by Down *et al.* in 2008. The high-throughput sequencing of the methylated DNA fragments produces a large number of short reads (36-50bp or 400 bp, depending on the technology). The short reads are aligned to a reference genome using alignment software such as Mapping and Assembly with Quality (Maq), which uses a Bayesian approach, along with base and mapping qualities to model error probabilities for the alignments. The reads can then be extended to represent the ~400 to 700 bp fragments from the sonication step. The coverage of these extended reads can be used to estimate the methylation level of the region. A genome browser such as Ensembl can also be used to visualize the data.

Validation of the approach to assess quality and accuracy of the data can be done with quantitative PCR. This is done by comparing a sequence from the MeDIP sample against an unmethylated control sequence. The samples are then run on a gel and the band intensities are compared. The relative intensity serves as the guide for finding enrichment. The results can also be compared with MeDIP-chip results to help determine coverage needed.

## Downstream bioinformatics analysis

The DNA methylation level estimations can be confounded by varying densities of methylated CpG sites across the genome when observing data generated by MeDIP. This can be problematic for analyzing CpG-poor (lower density) regions. One reason for this density issue is its effect on the efficiency of immunoprecipitation. In their study, Down *et al.* developed a tool to estimate absolute methylation levels from data generated by MeDIP by modeling the density of methylated CpG sites. This tool is called Bayesian tool for methylation analysis (Batman). The study reports the coverage of ~90% of all CpG sites in promoters, gene-coding regions, islands, and regulatory elements where methylation levels can be estimated; this is almost 20 times better coverage than any previous methods.

Studies using MeDIP-seq or MeDIP-chip are both genome-wide approaches that have the common aim of obtaining the functional mapping of the methylome. Once regions of DNA methylation are identified, a number of bioinformatics analyses can be applied to answer certain biological questions. One obvious step is to investigate genes contained in these regions and investigate the functional significance of their repression. For example, silencing of tumour-suppressor genes in cancer can be attributed to DNA methylation. By identifying mutational events leading to hypermethylation and subsequent repression of known tumour-suppressor genes, one can more specifically characterize the contributing factors to the cause of the disease. Alternatively, one can identify genes that are known to be normally methylated but, as a result of some mutation event, is no longer silenced.

Also, one can try and investigate and identify whether some epigenetic regulator has been affected such as DNA methyltransferase (DNMT); in these cases, enrichment may be more limited.

Gene-set analysis (for example using tools like DAVID and GoSeq) has been shown to be severely biased when applied to high-throughput methylation data (e.g. MeDIP-seq and MeDIP-ChIP); it has been suggested that this can be corrected using sample label permutations or using a statistical model to control for differences in the numberes of CpG probes / CpG sites that target each gene.

## Limitations of MeDIP

Limitations to take note when using MeDIP are typical experimental factors. This includes the quality and cross-reactivity of 5mC antibodies used in the procedure. Furthermore, DNA detection methods (i.e. array hybridization and high-throughput sequencing) typically involve well established limitations. Particularly for array-based procedures, as mentioned above, sequences being analyzed are limited to the specific array design used.

Most typical limitations to high-throughput, next generation sequencing apply. The problem of alignment accuracy to repetitive regions in the genome will result in less accurate analysis of methylation in those regions. Also, as was mentioned above, short reads (e.g. 36-50bp from an Illumina Genome Analyzer) represent a part of a sheared fragment when aligned to the genome; therefore, the exact methylation site can fall anywhere within a window that is a function of the fragment size. In this respect, bisulfite sequencing has much higher resolution (down to a single CpG site; single nucleotide level). However, this level of resolution may not be required for most applications, as the methylation status of CpG sites within \< 1000 bp has been shown to be significantly correlated.

## Applications of MeDIP

* Weber *et al.* 2005 determined that the inactive X-chromosome in females is hypermethylated on a chromosome wide level using MeDIP coupled with microarray.
* Keshet *et al.* 2006 performed a study on colon and prostate cancer cells using MeDIP-chip. The result is a genome-wide analysis of genes lying in hypermethylated regions as well as conclude that there is an instructive mechanism of de novo methylation in cancer cells.
* Zhang *et al.* 2006 obtained a high resolution methylome mapping in Arabidopsis using MeDIP-chip.
* Novak *et al.* 2006 used the MeDIP-chip approach to investigate human breast cancer for methylation associated silencing and observed the inactivation of the HOXA gene cluster


title: WKKS (AM)

abstract: WKKS is a radio station broadcasting a country music format. It is licensed to Vanceburg, Kentucky, United States. The station is currently owned by Brown Communications, Inc. WKKS 1570 AM plays classic country from the 1960s through the early 1990s. Common played stars include Ronnie Milsap, Waylon Jennings, Willie Nelson, Johnny Cash, Merle Haggard, Dan Seals, George Jones, Don Williams, Bellamy Brothers, and many other hits throughout that time period. The station focus is on country from the past and no newly released songs can be found there.

text:
# WKKS (AM)

**WKKS** (1570 AM) is a radio station broadcasting a country music format. It is licensed to Vanceburg, Kentucky, United States. The station is currently owned by Brown Communications, Inc.

WKKS 1570 AM plays classic country from the 1960s through the early 1990s. Common played stars include Ronnie Milsap, Waylon Jennings, Willie Nelson, Johnny Cash, Merle Haggard, Dan Seals, George Jones, Don Williams, Bellamy Brothers, and many other hits throughout that time period. The station focus is on country from the past and no newly released songs can be found there.

## InfoBox

WKKS
|  | |
| --- | --- |
| Frequency | 1570 kHz |
| Branding | *Kickin Country* |
| Programming | |
| Format | Country music |
| Ownership | |
| Owner | Brown Communications, Inc. |
| Technical information | |
| Licensing authority | FCC |
| Facility ID | 7319 |
| Class | D |
| Power | 1,000 watts day |
| Transmitter coordinates | 38°35′50″N 83°20′50″W / 38.59722°N 83.34722°W / 38.59722; -83.34722 |
| Links | |
| Public license information |  |
| Webcast | no |


title: 1979 Croke Cup

abstract: The 1979 Croke Cup was the 28th staging of the Croke Cup since its establishment by the Gaelic Athletic Association in 1944. The competition ran from 31 March to 29 April 1979. Templemore CBS were the defending champions, however, they were beaten by St Flannan's College in the Harty Cup semi-final. The final was played on 29 April 1979 at Semple Stadium in Thurles, between St Flannan's College and Presentation College, Birr, in what was their first ever meeting in the final. St Flannan's College won the match by 3–15 to 2–03 to claim a record-equalling seventh Croke Cup title and a first title in three years. Tom Howard was the top scorer with 2-06.

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# 1979 Croke Cup

The **1979 Croke Cup** was the 28th staging of the Croke Cup since its establishment by the Gaelic Athletic Association in 1944. The competition ran from 31 March to 29 April 1979.

Templemore CBS were the defending champions, however, they were beaten by St Flannan's College in the Harty Cup semi-final.

The final was played on 29 April 1979 at Semple Stadium in Thurles, between St Flannan's College and Presentation College, Birr, in what was their first ever meeting in the final. St Flannan's College won the match by 3–15 to 2–03 to claim a record-equalling seventh Croke Cup title and a first title in three years.

Tom Howard was the top scorer with 2-06.

## Qualification

| Province | Champions |
| --- | --- |
| Connacht | St Mary's College |
| Leinster | Presentation College, Birr |
| Munster | St Flannan's College |

## Results

### Semi-final

| 31 March 1979 Semi-final | **St Flannan's College** | **4-15 - 1-01** | **St Mary's College** | MacDonagh Park |
| --- | --- | --- | --- | --- |
|  | R Colleran 2-3, P Colleran 1-2, T Howard 0-5, J Morey 1-0, G Corry 0-3, G McInerney 0-1, M O'Grady 0-1. |  | P Burke 1-0, G Kilcommins 0-1. |  |

### Final

| 29 April 1979 Final | **St Flannan's College** | **3-15 - 2-03** | **Presentation College, Birr** | Semple Stadium |
| --- | --- | --- | --- | --- |
|  | T Howard 2-1, G McInerney 0-7, M O'Grady 1-0, R Colleran 0-2, P Colleran 0-2, S McMahon 0-1, G Corry 0-1. |  | J Verney 1-0, A Rosney 1-0, P Corrigan 0-2, J McLoughlin 0-1. |  |

## Statistics

### Top scorers

Overall

| Rank | Player | County | Tally | Total | Matches | Average |
| --- | --- | --- | --- | --- | --- | --- |
| 1 | Tom Howard | St Flannan's College | 2-06 | 12 | 2 | 6.00 |
| 2 | Ray Colleran | St Flannan's College | 2-05 | 11 | 2 | 5.50 |
| 3 | Gerry McInerney | St Flannan's College | 0-08 | 8 | 2 | 4.00 |

## InfoBox

1979 Croke Cup
| Dates | 31 March - 29 April 1979 |
| --- | --- |
| Teams | 3 |
| Champions | St Flannan's College (7th title)
Gerry McInerney (captain)
Séamus Gardiner (manager) |
| Runners-up | Presentation College, Birr
Joe Verney (captain)
Brother Denis (manager) |
| Tournament statistics | |
| Matches played | 2 |
| Goals scored | 10 (5 per match) |
| Points scored | 34 (17 per match) |
| Top scorer(s) | Tom Howard (2-06) |
| 1978 (Previous) (Next) 1980 | |