text:
Eleanor O'Brien
Modeling Humanities Data
3d Modelling, Analysis/Interpreting 3d Spaces
Digital Heritage: Theories, Methods and Challenges
Digital Humanities Practicum
April 20, 2017 3D Modelling, AFF625[A] Leave a comment
Day One: Visiting the Site (3d Modelling AFF625[A])
For my final project for this module on 3d modelling, I have decided to attempt to reconstruct the Lavabo at the Old Mellifont Abbey just outside Drogheda Co. Louth.
Mellifont was the first Cistercian monastery in Ireland, founded in 1142 by St Malachy of Armagh. Part of the reason why it is such an important site for the history of the country is the fact that it established the connection between Irish and continental church architecture. The first example for the Romanesque style was the construction of the church on the rock of Cashel in 1127. Just over a decade later the continental type of monastic design and planning was introduced at Mellifont, the first Cistercian abbey in Ireland. By the time it was dissolved in the beginning of the 16th century, Mellifont had become one of the richest monasteries in the country. Its most interesting architectural feature is the octagonal Lavabo built around the year 1200. This is also the most well preserved building on site. Today, very little of it is preserved of the site and with the Lavabo only 4 1/2 of the octangonal sides remain. A 3D reconstruction of the site would help to understand and see the grandeur of the Lavabo as it once was.
Before arriving to the site, from researching it and viewing images in books and online, I went in with the aim of reconstructing the whole site. After walking around the site for 5 minutes I knew that this was an impossible feat given the time constraints regarding the deadline.
Old Mellifont Abbey
Floor Plan of the Abbey [Source Old Mellifont Abbey]
The most intriguing structure on site is the Lavabo, where the monks would have originally washed their hands before meals. One of the reasons behind choosing this structure for my project is because although it is quite well preserved, there is a lot to consider when thinking about an interpretation. The structure, as you can see below still stands with 4 and 1/2 walls remaining.
One of the capitals at the Lavabo
Originally the middle of the Lavabo would have held the fountain, where the monks washed there hands. From Archival digs in 1953, remains of lead pipes were found which suggest that the fountain would have had 8 taps, as there were 8 pipes, which was what was traditional at the time. However there is no remains left of the fountain, one can assume that it would have been modeled off similar Cistercian Abbeys throughout Europe at the time, according to Roger Stalley in Decorating the Lavabo, it has been suggested that the fondant in the basement at Townley Hall was designed off the basins from Mellifont (the owners of Townley Hall also owning the Abbey at the time). The other option is to style or model it off the fondant at Poblet Monastary in Spain, also an eight taped fountain from a Cisterian Monastery built at the same time. So I will need to decide which is the most suited for the reconstruction.
Also another thing to consider is the second story of the Lavabo, this second story came later after the dissolution of the monasteries in the 16th century. Although there is no record of a roof, or even an interpretation of what it would have looked like, there is mention of a second storey, so this is another aspect of the structure I will need to consider.
Finally, I am hoping to in some way incorporate the medieval tiles into the Lavabo. These tiles can be found in the Chapter House currently, however as the original flooring was removed from the Lavabo, there is no reason why the tiles wouldn't have featured here, the Chapter house being only meters away, so I will have to consider this adaption.
Example of one of the style of tiles found at Mellifont
This and many more of my decisions and I'm sure failures when it comes to modelling the Lavabo will be coming up in later posts.
Roger Stalley Proceedings of the Royal Irish Academy. Section C: Archaeology, Celtic Studies, History, Linguistics, Literature. Vol. 96C, No.7 (1996), pp.237-264.
A Little Less Conversation, a Little More Action Please?
The migration of the aura and how we determine what is a good or bad copy.
Comparing Data Modelling Techniques
The Upper Floor.
The Fountain and the Tiles.
Deirdre Power on A Little Less Conversation, a Little More Action Please?
Sarah-Louise Roche on A Little Less Conversation, a Little More Action Please?
AFF604A[A]
AFF625[A]
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text:
The Nitol botnet mostly involved in spreading malware and distributed denial-of-service attacks.

History
The Nitol Botnet was first discovered around December 2012, with analysis of the botnet indicating that the botnet is mostly prevalent in China where an estimate 85% of the infections are detected. In China the botnet was found to be present on systems that came brand-new from the factory, indicating the trojan was installed somewhere during the assembly and manufacturing process. According to Microsoft the systems at risk also contained a counterfeit installation of Microsoft Windows.

On 10 September 2012 Microsoft took action against the Nitol Botnet by obtaining a court order and subsequently sinkholing the 3322.org domain. The 3322.org domain is a Dynamic DNS which was used by the botnet creators as a command and control infrastructure for controlling their botnet. Microsoft later settled with 3322.org operator Pen Yong, which allowed the latter to continue operating the domain on the condition that any subdomains linked to malware remain sinkholed.

See also
Internet crime
Internet security

References

External links
 Analysis of the Nitol Botnet, created by Microsoft as part of Operation b70

Internet security
Distributed computing projects
Spamming
Botnets

redpajama_set_name: RedPajamaWikipedia


Trump: "It was all lies and it was fiction"
Republican presidential nominee Donald Trump said allegations of personal misconduct were ''lies and fiction,'' in the final presidential debate. Rough Cut (no reporter narration).
ROUGH CUT (NO REPORTER NARRATION) STORY: Republican presidential nominee Donald Trump said allegations of personal misconduct were "lies and fiction," in the final presidential debate. Trump has been damaged recently by several accusations of groping women - which he denies - and concerns about his claims that the election will be rigged against him. Clinton said, "he held a number of big rallies where he said he could not possibly have done those things, to those women, because they were not attractive enough" Trump interjected saying, "I did not say that." The debate at the University of Las Vegas Nevada gives the New York businessman perhaps his best remaining chance to sway the dwindling number of Americans who are still undecided about which way to vote in the Nov. 8 election. For Clinton, who leads national polls and in most of the battleground states where the election will likely be decided, the 90-minute debate is a chance to make a closing argument on why she is best suited to succeed President Barack Obama. Tens of millions of voters are expected to tune in.


text:
Genetic Alliance UK /
We're hiring: Director of Fundraising and Business Development
Last Reviewed 28/03/2017
We're looking for someone to join our team as our new Director of Fundraising and Business Development. This is an exciting opportunity for an outstanding candidate to support Genetic Alliance UK to maintain and develop its position as a sector leader.
Click here to look at the job pack for this role.
Job title: Director of Fundraising and Business Development
Responsible to: Executive Director
Responsible for: Fundraising Manager and Fundraising Officer
Salary: £40,000 ― £45,000 per annum, depending upon experience
Benefits: 33 paid holiday days per year, plus contribution to pension
Contract: 12 months (with potential for extension), full-time
Located: 37 Queen Square, London, WC1N 3BH
Develop and implement a robust organisational fundraising and income generation strategy.
Support Genetic Alliance UK to maintain and develop its position as a sector leader by securing new income and developing new income streams.
Successfully manage existing industry and corporate relationships and cultivate new partnerships.
Lead and develop a motivated fundraising team. The successful candidate will be responsible for designing the remit and recruiting a Fundraising Manager (a new role).
Contribute to the development of the organisation working closely with the senior management team.
Principle duties
Develop a robust fundraising strategy to support the growth and development of Genetic Alliance UK.
Develop organisational cases for support, tailored to relevant audiences.
To raise the profile of the Genetic Alliance UK charity and identify, develop and access funding opportunities through networking and partnerships at a senior level with large corporations, public sector organisations, trusts and foundations and other organisations working within the fields of health and biomedical research.
To work with Genetic Alliance UK staff, trustees and members to transform ideas and priorities into fundable projects and activities.
To confidently develop and deliver high quality pitches to potential funders and supporters.
Oversee the development and submission of clear, detailed funding applications and proposals to public, corporate, trust and foundations.
Work with colleagues to ensure the monitoring and evaluation of projects and activities is undertaken in accordance with funder and commissioner requirements.
To oversee the submission of relevant reporting of outcomes to funders and commissioners.
To support and manage the development of Genetic Alliance UK's fundraising team.
Work with the Senior Management Team to contribute to the development of the organisation's strategy, sharing responsibility for the overall management of the organisation.
Educated to degree level or equivalent.
At least 2 years' experience in a similar role.
Successful track record in fundraising at a senior level engaging with corporate and industry supporters.
Experience of building cases for support in complex organisations and developing fundraising strategies covering diverse income streams.
Experience of developing detailed trust and grant applications.
Experience of securing funds for charities working in the fields of health and/or medicine.
Experience of securing funds for infrastructure, policy and campaigning organisations.
Personal skills and attributes
Creative, innovative and enthusiastic.
Commitment to the values and core mission of Genetic Alliance UK.
A positive approach to addressing the issues faced by patients and families affected by rare and genetic conditions.
Team based, collaborative approach.
Target driven with attention to detail.
Please email your CV and an accompanying cover letter to [email protected] with the subject heading 'Director of Fundraising and Business Development.'
5pm, Thursday 13 April 2017
To view the job pack for this role please click here.

redpajama_set_name: RedPajamaCommonCrawl


text:
package org.scalactic.anyvals

import org.scalatest._
import org.scalatest.prop.PropertyChecks
// SKIP-SCALATESTJS,NATIVE-START
import scala.collection.immutable.NumericRange
// SKIP-SCALATESTJS,NATIVE-END
import OptionValues._
import scala.collection.mutable.WrappedArray
//import org.scalactic.StrictCheckedEquality
import Double.NaN
import org.scalactic.Equality
import org.scalactic.{Pass, Fail}
import org.scalactic.{Good, Bad}
import scala.util.{Try, Success, Failure}

trait PosZFiniteDoubleSpecSupport {

  implicit val doubleEquality: Equality[Double] =
    new Equality[Double] {
      override def areEqual(a: Double, b: Any): Boolean =
        (a, b) match {
          case (a, bDouble: Double) if a.isNaN && bDouble.isNaN  => true
          case _ => a == b
        }
    }

  implicit val floatEquality: Equality[Float] =
    new Equality[Float] {
      override def areEqual(a: Float, b: Any): Boolean =
        (a, b) match {
          case (a, bFloat: Float) if a.isNaN && bFloat.isNaN => true
          case _ => a == b
        }
    }

  implicit def tryEquality[T]: Equality[Try[T]] = new Equality[Try[T]] {
    override def areEqual(a: Try[T], b: Any): Boolean = a match {
      case Success(double: Double) if double.isNaN =>  // This is because in scala.js x/0 results to NaN not ArithmetricException like in jvm, and we need to make sure Success(NaN) == Success(NaN) is true to pass the test.
        b match {
          case Success(bDouble: Double) if bDouble.isNaN => true
          case _ => false
        }
      case _: Success[_] => a == b
      case Failure(ex) => b match {
        case _: Success[_] => false
        case Failure(otherEx) => ex.getClass == otherEx.getClass && ex.getMessage == otherEx.getMessage
        case _ => false
      }
    }
  }

}

class PosZFiniteDoubleSpec extends funspec.AnyFunSpec with matchers.should.Matchers with PropertyChecks with PosZFiniteDoubleSpecSupport {

  describe("A PosZFiniteDouble") {
    describe("should offer a from factory method that") {
      it("returns Some[PosZFiniteDouble] if the passed Double is greater than or equal to 0") {
        PosZFiniteDouble.from(0.0).value.value shouldBe 0.0
        PosZFiniteDouble.from(50.23).value.value shouldBe 50.23
        PosZFiniteDouble.from(100.0).value.value shouldBe 100.0
      }
      it("returns None if the passed Double is NOT greater than or equal to 0") {
        PosZFiniteDouble.from(-0.00001) shouldBe None
        PosZFiniteDouble.from(-99.9) shouldBe None
      }
    }
    describe("should offer an ensuringValid factory method that") {
      it("returns PosZFiniteDouble if the passed Double is greater than or equal to 0") {
        PosZFiniteDouble.ensuringValid(0.0).value shouldBe 0.0
        PosZFiniteDouble.ensuringValid(50.23).value shouldBe 50.23
        PosZFiniteDouble.ensuringValid(100.0).value shouldBe 100.0
      }
      it("throws AssertionError if the passed Double is NOT greater than or equal to 0") {
        an [AssertionError] should be thrownBy PosZFiniteDouble.ensuringValid(-0.00001)
        an [AssertionError] should be thrownBy PosZFiniteDouble.ensuringValid(-99.9)
        an [AssertionError] should be thrownBy PosZFiniteDouble.ensuringValid(Double.PositiveInfinity)
        an [AssertionError] should be thrownBy PosZFiniteDouble.ensuringValid(Double.NegativeInfinity)
        // SKIP-DOTTY-START
        // https://github.com/lampepfl/dotty/issues/6710
        an [AssertionError] should be thrownBy PosZFiniteDouble.ensuringValid(Double.NaN)
        // SKIP-DOTTY-END
      }
    }
    describe("should offer a tryingValid factory method that") {
      import TryValues._
      it("returns a PosZFiniteDouble wrapped in a Success if the passed Double is greater than or equal 0") {
        PosZFiniteDouble.tryingValid(0.0).success.value.value shouldBe 0.0
        PosZFiniteDouble.tryingValid(50.0).success.value.value shouldBe 50.0
        PosZFiniteDouble.tryingValid(100.0f).success.value.value shouldBe 100.0
      }

      it("returns an AssertionError wrapped in a Failure if the passed Double is lesser than 0") {
        PosZFiniteDouble.tryingValid(-1.0).failure.exception shouldBe an [AssertionError]
        PosZFiniteDouble.tryingValid(-99.0).failure.exception shouldBe an [AssertionError]
      }
    }
    describe("should offer a passOrElse factory method that") {
      it("returns a Pass if the given Double is greater than or equal 0") {
        PosZFiniteDouble.passOrElse(0.0)(i => i) shouldBe Pass
        PosZFiniteDouble.passOrElse(50.0)(i => i) shouldBe Pass
        PosZFiniteDouble.passOrElse(100.0)(i => i) shouldBe Pass
      }
      it("returns an error value produced by passing the given Double to the given function if the passed Double is lesser than 0, wrapped in a Fail") {
        PosZFiniteDouble.passOrElse(-1.0)(i => i) shouldBe Fail(-1.0)
        PosZFiniteDouble.passOrElse(-99.0)(i => i + 3.0) shouldBe Fail(-96.0)
      }
    }
    describe("should offer a goodOrElse factory method that") {
      it("returns a PosZFiniteDouble wrapped in a Good if the given Double is greater than or equal 0") {
        PosZFiniteDouble.goodOrElse(0.0)(i => i) shouldBe Good(PosZFiniteDouble(0.0))
        PosZFiniteDouble.goodOrElse(50.0)(i => i) shouldBe Good(PosZFiniteDouble(50.0))
        PosZFiniteDouble.goodOrElse(100.0)(i => i) shouldBe Good(PosZFiniteDouble(100.0))
      }
      it("returns an error value produced by passing the given Double to the given function if the passed Double is lesser than 0, wrapped in a Bad") {
        PosZFiniteDouble.goodOrElse(-1.0)(i => i) shouldBe Bad(-1.0)
        PosZFiniteDouble.goodOrElse(-99.0)(i => i + 3.0f) shouldBe Bad(-96.0)
      }
    }
    describe("should offer a rightOrElse factory method that") {
      it("returns a PosZFiniteDouble wrapped in a Right if the given Double is greater than or equal 0") {
        PosZFiniteDouble.rightOrElse(0.0)(i => i) shouldBe Right(PosZFiniteDouble(0.0))
        PosZFiniteDouble.rightOrElse(50.0)(i => i) shouldBe Right(PosZFiniteDouble(50.0))
        PosZFiniteDouble.rightOrElse(100.0)(i => i) shouldBe Right(PosZFiniteDouble(100.0))
      }
      it("returns an error value produced by passing the given Double to the given function if the passed Double is lesser than 0, wrapped in a Left") {
        PosZFiniteDouble.rightOrElse(-1.0)(i => i) shouldBe Left(-1.0)
        PosZFiniteDouble.rightOrElse(-99.0)(i => i + 3.0f) shouldBe Left(-96.0)
      }
    }
    describe("should offer an isValid predicate method that") {
      it("returns true if the passed Double is greater than or equal to 0") {
        PosZFiniteDouble.isValid(50.23) shouldBe true
        PosZFiniteDouble.isValid(100.0) shouldBe true
        PosZFiniteDouble.isValid(0.0) shouldBe true
        PosZFiniteDouble.isValid(-0.0) shouldBe true
        PosZFiniteDouble.isValid(-0.00001) shouldBe false
        PosZFiniteDouble.isValid(-99.9) shouldBe false
      }
    }
    describe("should offer a fromOrElse factory method that") {
      it("returns a PosZFiniteDouble if the passed Double is greater than or equal to 0") {
        PosZFiniteDouble.fromOrElse(50.23, PosZFiniteDouble(42.0)).value shouldBe 50.23
        PosZFiniteDouble.fromOrElse(100.0, PosZFiniteDouble(42.0)).value shouldBe 100.0
        PosZFiniteDouble.fromOrElse(0.0, PosZFiniteDouble(42.0)).value shouldBe 0.0
      }
      it("returns a given default if the passed Double is NOT greater than or equal to 0") {
        PosZFiniteDouble.fromOrElse(-0.00001, PosZFiniteDouble(42.0)).value shouldBe 42.0
        PosZFiniteDouble.fromOrElse(-99.9, PosZFiniteDouble(42.0)).value shouldBe 42.0
      }
    }
    it("should offer MaxValue, MinValue, and MinPositiveValue factory methods") {
      PosZFiniteDouble.MaxValue shouldEqual PosZFiniteDouble.from(Double.MaxValue).get
      PosZFiniteDouble.MinValue shouldEqual PosZFiniteDouble(0.0)
      PosZFiniteDouble.MinPositiveValue shouldEqual
        PosZFiniteDouble.from(Double.MinPositiveValue).get
    }
    it("should not offer a PositiveInfinity factory method") {
      "PosZFiniteDouble.PositiveInfinity" shouldNot compile
    }
    it("should not offer a NegativeInfinity factory method") {
      "PosZFiniteDouble.NegativeInfinity" shouldNot compile
    }
/* This now compiles because of the newly added implicit PosZFiniteDouble => PosZDouble method
    PosZFiniteDouble(1.0f).isPosInfinity
*/
    it("should not offer a isNegInfinity method") {
      "PosZFiniteDouble(1.0f).isNegInfinity" shouldNot compile
    }

    it("should be sortable") {
      val xs = List(PosZFiniteDouble(2.2), PosZFiniteDouble(0.0), PosZFiniteDouble(1.1),
        PosZFiniteDouble(3.3))
      xs.sorted shouldEqual List(PosZFiniteDouble(0.0), PosZFiniteDouble(1.1),
        PosZFiniteDouble(2.2), PosZFiniteDouble(3.3))
    }

    describe("when created with apply method") {

      it("should compile when 8 is passed in") {
        "PosZFiniteDouble(8)" should compile
        PosZFiniteDouble(8).value shouldEqual 8.0
        "PosZFiniteDouble(8L)" should compile
        PosZFiniteDouble(8L).value shouldEqual 8.0
        "PosZFiniteDouble(8.0F)" should compile
        PosZFiniteDouble(8.0F).value shouldEqual 8.0
        "PosZFiniteDouble(8.0)" should compile
        PosZFiniteDouble(8.0).value shouldEqual 8.0
      }

      it("should compile when 0 is passed in") {
        "PosZFiniteDouble(0)" should compile
        PosZFiniteDouble(0).value shouldEqual 0.0
        "PosZFiniteDouble(0L)" should compile
        PosZFiniteDouble(0L).value shouldEqual 0.0
        "PosZFiniteDouble(0.0F)" should compile
        PosZFiniteDouble(0.0F).value shouldEqual 0.0
        "PosZFiniteDouble(0.0)" should compile
        PosZFiniteDouble(0.0).value shouldEqual 0.0
      }

      it("should not compile when -8 is passed in") {
        "PosZFiniteDouble(-8)" shouldNot compile
        "PosZFiniteDouble(-8L)" shouldNot compile
        "PosZFiniteDouble(-8.0F)" shouldNot compile
        "PosZFiniteDouble(-8.0)" shouldNot compile
      }
      it("should not compile when x is passed in") {
        val a: Int = -8
        "PosZFiniteDouble(a)" shouldNot compile
        val b: Long = -8L
        "PosZFiniteDouble(b)" shouldNot compile
        val c: Float = -8.0F
        "PosZFiniteDouble(c)" shouldNot compile
        val d: Double = -8.0
        "PosZFiniteDouble(d)" shouldNot compile
      }
    }
    describe("when specified as a plain-old Double") {

      def takesPosZFiniteDouble(poz: PosZFiniteDouble): Double = poz.value

      it("should compile when 8 is passed in") {
        "takesPosZFiniteDouble(8)" should compile
        takesPosZFiniteDouble(8) shouldEqual 8.0
        "takesPosZFiniteDouble(8L)" should compile
        takesPosZFiniteDouble(8L) shouldEqual 8.0
        "takesPosZFiniteDouble(8.0F)" should compile
        takesPosZFiniteDouble(8.0F) shouldEqual 8.0
        "takesPosZFiniteDouble(8.0)" should compile
        takesPosZFiniteDouble(8.0) shouldEqual 8.0
      }

      it("should compile when 0 is passed in") {
        "takesPosZFiniteDouble(0)" should compile
        takesPosZFiniteDouble(0) shouldEqual 0.0
        "takesPosZFiniteDouble(0L)" should compile
        takesPosZFiniteDouble(0L) shouldEqual 0.0
        "takesPosZFiniteDouble(0.0F)" should compile
        takesPosZFiniteDouble(0.0F) shouldEqual 0.0
        "takesPosZFiniteDouble(0.0)" should compile
        takesPosZFiniteDouble(0.0) shouldEqual 0.0
      }

      it("should not compile when -8 is passed in") {
        "takesPosZFiniteDouble(-8)" shouldNot compile
        "takesPosZFiniteDouble(-8L)" shouldNot compile
        "takesPosZFiniteDouble(-8.0F)" shouldNot compile
        "takesPosZFiniteDouble(-8.0)" shouldNot compile
      }

      it("should not compile when x is passed in") {
        val x: Int = -8
        "takesPosZFiniteDouble(x)" shouldNot compile
        val b: Long = -8L
        "takesPosZFiniteDouble(b)" shouldNot compile
        val c: Float = -8.0F
        "takesPosZFiniteDouble(c)" shouldNot compile
        val d: Double = -8.0
        "takesPosZFiniteDouble(d)" shouldNot compile
      }
    }

    it("should offer a unary + method that is consistent with Double") {
      forAll { (p: PosZFiniteDouble) =>
        (+p).toDouble shouldEqual (+(p.toDouble))
      }
    }

    it("should offer a unary - method that returns NegZFiniteDouble") {
      forAll { (p: PosZFiniteDouble) =>
        (-p) shouldEqual (NegZFiniteDouble.ensuringValid(-(p.toDouble)))
      }
    }

    it("should offer 'min' and 'max' methods that are consistent with Double") {
      forAll { (pzdouble1: PosZFiniteDouble, pzdouble2: PosZFiniteDouble) =>
        pzdouble1.max(pzdouble2).toDouble shouldEqual pzdouble1.toDouble.max(pzdouble2.toDouble)
        pzdouble1.min(pzdouble2).toDouble shouldEqual pzdouble1.toDouble.min(pzdouble2.toDouble)
      }
    }

    it("should offer an 'isWhole' method that is consistent with Double") {
      forAll { (pzdouble: PosZFiniteDouble) =>
        pzdouble.isWhole shouldEqual pzdouble.toDouble.isWhole
      }
    }

    it("should offer 'round', 'ceil', and 'floor' methods that are consistent with Double") {
      forAll { (pzdouble: PosZFiniteDouble) =>
        pzdouble.round.toDouble shouldEqual pzdouble.toDouble.round
        pzdouble.ceil.toDouble shouldEqual pzdouble.toDouble.ceil
        pzdouble.floor.toDouble shouldEqual pzdouble.toDouble.floor
      }
    }

    it("should offer 'toRadians' and 'toDegrees' methods that are consistent with Double") {
      forAll { (pzdouble: PosZFiniteDouble) =>
        pzdouble.toRadians shouldEqual pzdouble.toDouble.toRadians
      }
    }

    it("should offer widening methods for basic types that are consistent with Double") {
      forAll { (pzdouble: PosZFiniteDouble) =>
        def widen(value: Double): Double = value
        widen(pzdouble) shouldEqual widen(pzdouble.toDouble)
      }
    }
    it("should offer an ensuringValid method that takes a Double => Double, throwing AssertionError if the result is invalid") {
      PosZFiniteDouble(33.0).ensuringValid(_ + 1.0) shouldEqual PosZFiniteDouble(34.0)
      an [AssertionError] should be thrownBy { PosZFiniteDouble.MaxValue.ensuringValid(_ - PosZFiniteDouble.MaxValue - 1) }
      an [AssertionError] should be thrownBy { PosZFiniteDouble.MaxValue.ensuringValid(_ => Double.PositiveInfinity) }
      an [AssertionError] should be thrownBy { PosZFiniteDouble.MaxValue.ensuringValid(_ => Double.NegativeInfinity) }
      // SKIP-DOTTY-START
      // https://github.com/lampepfl/dotty/issues/6710
      an [AssertionError] should be thrownBy { PosZFiniteDouble.MaxValue.ensuringValid(_ => Double.NaN) }
      // SKIP-DOTTY-END
    }
  }
}

redpajama_set_name: RedPajamaGithub


text:
Aarhus Mølle (Aarhus Mill) is a building in Aarhus, Denmark. The mill dates back to at least 1289 but the oldest of the existing buildings are from the 1600s while the main building is from c. 1700. The building complex comprise three buildings; a main building from c. 1700, a stables from the 1600s and a malt mill from 1782. Originally constructed on Vestergade in the Indre by neighborhood it has since been moved to the Old Town Museum where it is now used as the main administrative building and for some museum-related workshops.

Many places in Aarhus has been named for the mill; the Aarhus river used to be called Mølleåen (Mill-river) and there was a large pond by the mill known as Mølledammen (Mill pond). The city gate Mølleport (Mill Gate) lay on the corner of Vester Alle and Vestergade. Until 1910 a part of Vestergade was called Møllegade (Mill Street). Present day Mølleparken (Mill Park) was created on the old pond used by the mill.

History
Aarhus Mill was built at some point in the early Middle Ages. The exact date is not known but it is mentioned for the first time in records from 1289 and later in 1581 when a new mill was built. The mill was built on the Aarhus river west of Aarhus and east of Brabrand Lake and was mainly used for malt and flour production. In the later Middle Ages it became illegal to mill products privately and farmers were forced to use one of the official, royally recognized mills, including Aarhus Mill.

In 1861 the mill was converted from water power to steam power but a few years later, in 1873, the flour production stopped as machines became more common during the Industrial Revolution. The mill remained in use to some extent until 1913. In 1926 the mill was bequeathed to the Old Town Museum when the last owner of it died. The four main buildings were moved to the Old Town in 1928 and today houses the administration and several workshops.

In 1849 one of the buildings burned down and during the cleanup a rune stone was discovered in the foundation. The stone was salvaged and is today displayed at Moesgård Museum which also uses the motif of the stone as its logo. The stone is known as "Aarhusstenen" (The Aarhus Stone) or "Maskestenen" (The Mask Stone).

Architecture
The main building is from around 1700, designed with Baroque style elements. It is a half-timbered structure designed with two lower wall studs and one upper stud which was typical for the early Baroque in the Danish provincial cities in Jutland. The pronounced cornice is also characteristic for Baroque buildings. The color palette of grey-blue lumber with yellow panels and red joints are from around 1800.

Owners
 1289-????: ????
 1581-????: Anders Possin
 1644–1753: Jens Jensen and Marie Wissing
 1753-????: Christian Henrich Grotum and Jens Wissings enke.
 ????-1773: Lars Christian Meulengracht (????-1773)
 1790–1793: Frederik Christian Dahl and Christian Faurschou
 1793–1805: Frederik Christian Dahl
 1805–1815: Johannes Dahl
 1815–1817: Kjerstine Dahl
 1817–1839: Christian Guldager, married Kjerstine Dahl
 1839–1846: Kirstine Dahl
 1846–1889: Andreas Severin Weis
 1889–1912: Ernst August Weis
 1912–1926: Wilhelmine Weis
 1926–present: Old Town Museum

References

Buildings and structures in Aarhus


Celica was originally designed for motorists motorists who love fun and style, and more than just a simple means of transportation.
The name is derived from the Latin word célico meaning "from the heavens" or "celestial".
Through all generations, Celicas have been built around Toyota's high-performance inline-4 engines.
The plans for the Celica started in 1967.
The first generation Celica was released to the market in 1970,at 1970 Tokyo Motor Show in October.It was a "cut-down" version of Toyota's supercar, the 2000GT, so it was a relatively affordable sports car.
Based on the EX-1 "Car of the Future" prototype, its styling was quite revolutionary for the day.
The Celica was Toyota's version of the Mustang - an image car rather than a high-volume car.
The first generation came out in two different versions, the LT and ST.
The lower-end LT was equipped with a 2T carbureted four-cylinder engine displacing 1600 cc, while the ST came with a twin Solex-carburetor 2T-B engine.
The Celica sold well from the outset, its first major change or addition taking place in 1974 with the addition of the GT model.The 2T-G that powered the high-end GT model was a DOHC twin-Solex carburetor 1600 cc engine.
The GT model came with various upgrades like underbody spoilers, tinted windows, different hood flutes, power windows, air conditioning, GT front grill, and shared a few things with the ST - a full-length center console and oil pressure/ammeter gauges, rather than the LT's warning lights.
In 1974, 1976 and 1977 Celica wins Motor Trend "Import Car of the Year."
In 1976, the Celica line was enlarged with the addition of the liftback model, available only in GT trim.The Liftback was introduced for Japanese market in April 1973, but not until 1976 for North America.
The GT package included the larger engine, offered sportier handling and a higher-grade trim. This model was marketed as a sport-touring type vehicle, offering greater comfort and luggage capacity than the standard models.
The first Celica for North America, 1971 ST was powered by 1.9 liter 8R engine. The 1972-1974 models have 2.0 liter 18R engine. For 1975-1977, engine for the North American Celica is 2.2 liter 20R. The Celica GT and LT models were introduced in the U.S. for the 1974 model year. The top-line GT included a 5-speed manual transmission, rocker panel GT stripes, and styled steel wheels with chrome trim rings. The LT was marketed as an economy model. Mid-1974 saw minor changes in the Celica's trim and badges.
In June 1977 Celica reache one million models produced.
The very first entry for Celica in the World Rally Championship was in 1972 RAC Rally when Ove Andersson drove TA22 1600GTV into the ninth place.
The second generation Celica was released in 1978,(production began in late 1977) and was again available in both ST and GT trim levels.
Power was provided by 2.2-liter engines for both models. This new generation offered more safety, power and economy than previous models, and was awarded Motor Trend's "Import Car of the Year" for 1978.
The second generation Celica can be broken down into two series of release (known as Series A and Series B). These two Celica's were only distinguishable by appearance, both having the same engine capacity. Series A Celica's (1977-1979) were released with round headlights and chrome bumpers for lower grades. The higher grades such as GT has black rubber bumpers. The Series B Celica (1980-1981) was released with square headlights and Black rubber bumpers and various other 'minor' differences.
In 1980, a four-door version was announced, known as the Toyota Celica Camry. This model was a Toyota Carina with a Celica front end. The Camry was spun off as its own model two years later.
The limited edition "US Grand Prix" GT Liftback was offered in 1980, and in 1981 the GTA Coupe was released to celebrate the Celica 10th Anniversary.
There were about 70 different models of 2nd generation Celica ever sold in Japan.
The third generation came in production in 1982.
Styling was changed considerably from previous models and power was now provided by 2.4-liter engines.
In 1983, Toyota added the GT-S model to the Celica line to re-inject the sports image that Celica had lost as it grew larger and heavier with each subsequent model. The GT-S included larger wheels and tires, fender flares, sports suspension, and a sports interior including special seats and a leather-wrapped steering-wheel and gearshift knob.
Minor changes were given in late 1983 for 1984 model year, and distinguished by the redesigned front end, with fully-closed retractable headlights. Side vents, Hood, grille, tail lights,and bumpers were also new. The GT-R and GT-TR (turbo) were added to the Japanese line up.
Fuel injection became standard on all North American Celica, therefore the 22R engine became 22R-E. The GT-S Convertible, built by American Sunroof Corporation in California, was released in 1984.
In the year 1986 the Celica changed completly.
It was now an all-new vehicle with front wheel drive, a rounded, flowing body and new 2.0 L four-cylinder engines. In North America, the Celica was now available in ST, GT and GT-S trim, all available as either coupe or liftback models, with the GT being offered up in a soft-top convertible coupe as well.
STs and GTs came with a 116-horsepower engine, while the GT-S was given a 135-horsepower version of the same 2.0-liter engine. Front-wheel-drive and four-wheel independent suspension made the Celica the perfect all-around sports car.
For Japanese market Toyota introduced the "ultimate Celica", the GT-Four (ST165) in October 1986. With full-time all wheel drive and a turbocharged version of the GT-S 2.0 L engine producing 190 hp (3S-GTE), it immediately took its place as the flagship of the Celica range, and became the official Toyota rally car for all years of production. The GT-Four began exporting for 1988 model year, and marketed in the USA as All-trac Turbo.
In 1988, the ST163 with 4S-Fi engine was added into Japanese line up in ST and SX trim levels.
The ST165 GT-Four made its World Rally debut in 1988 Tour de Corse and finished 6th. The first victory came in 1988 Cyprus (non-WRC), and the first WRC victory in 1989 Rally Australia.
The fifth generation Celica was introduced in September 1989.They received revised styling, upgraded wheels and tires, and more power.
Anti-lock brakes were available on all models, as were numerous luxury items — all were standard on the All-Trac model though. With its leather interior, ten-speaker sound1990 Toyota Celica All-Trac system and power-operated driver's seat and sunroof included as standard equipment, the All-Trac was the most expensive Celica yet. With its 200-horsepower turbocharged engine, it was also the most powerful Celica yet.
Japanese domestic market models are S-R, Z-R, GT-R, Active Sports (with active suspension), and GT-Four.
In North America, the GT and GT-S were powered by the 2.2 L 5S-FE, while the ST sported the DOHC 16-valve, 1.6 L 4A-FE. Celica for North America has aero (non-folding) door mirrors, and amber front corner lights.
Trim levels for Europe are 1.6 ST-i, 2.0 GT-i 16, and GT-Four. The 2.0 GT-i 16 Cabriolet was offered only in certain European countries. Models for Australia are SX Coupe, SX Liftback, GT-Four and also 150 units limited edition GT-Four Group A Rallye.
In August 1990, the GT-Four A and Convertible were added into Japanese line up. Super Live Sound System with 10-speakers is standard on the GT-Four A, and optional in other models, but S-R. The 20th Anniversary GT-R came in December 1990 to celebrate 20 years of Celica.
* different bumper which is much lighter than the standard one.
In August 1991 for 1992 model year Toyota facelifted the Celica.
The Celica was only available in ST and GT trims in the US for the 1994 model year, but the addition of the optional "sports package" to the GT produced GT-S-like handling. The ST has new 1.8 liter 7A-FE engine, the GT is powered by a 2.2 liter 5S-FE. Styling of the new Celicas was acclaimed by most publications as "Supra-esque" with four exposed headlights. Celicas were available in either coupe or liftback form, with the GT sports package available only on the liftback. New safety equipment in the form of driver (and then later passenger-side) airbags was standard, and anti-lock brakes were available on all models. Many Celicas also sported CFC-free air conditioning.
Production of the All-Trac, or GT-Four as it was known outside the US, continued for the Japanese, Australian, European, and British markets. This version was to be the most powerful Celica produced to date, producing between 240-250 hp from an updated 3S-GTE engine. Influenced strongly by Team Toyota Europe, Toyota's factory team in the World Rally Championship, the final version of the GT-Four included improvements such as an all aluminum hood to save weight, four-channel ABS, an improved CT20B turbocharger, and Super Strut Suspension. The 2500 homologation cars built to allow Toyota to enter the GT-Four as a Group A car in the World Rally Championship also sported extras such as all of the plumbing required to activate an anti-lag system, a water spray bar for the front Intercooler and an extender spoiler mounted on risers. The car proved to be quite competitive in the 1995 World Championship. However, the team was banned from competition for a year after the car's single victory due to turbocharger irregularities.
The 1996 Celica received optional side skirts to improve its aerodynamic efficiency, as well as a redesigned rear spoiler. Also available were optional driving lights in the redesigned grille area (standard on GT models). To celebrate 25 years of Celica, the SS-I and SS-III Special Edition were released in Japan, and the 25th Anniversary ST Limited and GT Convertible marked this occasion in the USA.
In 1998, the ST model was discontinued to simplify the Celica ordering process. All Celicas in North America (coupe, liftback and convertible) were now GT models.
The 1998 models have 3 spoke sporty steering wheel and the deletion of front strut bar. Based on the 1.8 ST, Toyota GB released the Celica SR with lowered suspension, bigger alloys, and mesh grille.
In 1999, the Celica lineup was simplified even further with the elimination of the coupe model. The Celica was now available as a GT Liftback or a GT Convertible. The GT-Four was still offered in Japan. Also in 1999, Toyota released pictures of their next concept car, dubbed the XYR. The XYR displayed an aggressive stance and radical styling not seen since the last Toyota sports car, the Supra.
In 2000, Toyota began production of the seventh generation Celica. It was very close to the XYR concept with the exception of the front bumper and rear spoiler. The 2000 Celica was an element of Toyota Project Genesis, an effort to bring younger buyers to the marque in the United States.
This Celica came in two trim levels, the GT powered by an economical 1.8 L 4-cylinder 140 hp engine and the GT-S powered by a higher-performance 1.8 L 4-cylinder 180 hp version, co-developed with Yamaha. Both of these engines featured Toyota's signature VVT-i (Variable Valve Timing with Intelligence) system, which continuously varies the camshaft timing. The GT-S had a more aggressive system called the VVTL-i (Variable Valve Timing with Lift and Intelligence), which is similar to the VVT-i except until 6200 rpm, when valve lift is increased a fraction further to provide an abrupt increase in power, accounting for the 40 hp difference. The GT was available in both a 5-speed manual and 4-speed automatic and the GT-S was available with a close-ratio 6-speed manual and a 4-speed manumatic.
In 2001, Honda released its Integra replacement, the Acura RSX, for the 2002 model year with a 2.0 L 4-cylinder 200 hp engine, which competed directly with the Celica.
In 2002 Toyota also made some changes on the Celica GT-S, with the revs being limited to 7800 rpm, down from 8350 rpm on the original 7th generation.
In 2003 the Celica received a face lift, with a revised front bumper, revised tail lights, and the addition of several new colors to the lineup. The GT-S was also now equipped with a drive-by-wire throttle body in the manual transmission model. Throttle drive-by-wire, while shortening throttle response, comprimises the ability to use an aftermarket ECU, thus limiting tuning potential.
In July 2004, Toyota announced the Celica (as well as the MR2) would be discontinued in the United States at the end of the 2005 model year because of increasing competition and lack of sales.
The last Celica was rolled off production line on April 21, 2006.
In the late 1988-1996 Toyota won several WRC championships in a modified GT-4 Celica driven by Carlos Saintz. With an extremely modified engine, X-Trac transmission the Toyota Celica was always a contender throughout its WRC history winning 38 WRC Rallies and 2 WRC Championships.
Toyota began getting involved in WRC with the introduction of the Celica GT-4 (or All-Trac in the States) in 1988. With introduction of the GT-4 and sales of between 2500-5000 production versions worldwide a year Toyota was eligible to race in WRC. Toyota campaigned in both the 4, 5th and 6th Generation GT-4...however titles were won in the 5th generation Celica. The fifth generation car was perfect for rally at the time, however problems with the hood scoop aerodynamics forced a mid-generation addition of the Rally/Group A/RC edition. The Celica RC had a recessed hood vent instead of a hood scoop, and added an improved turbo and intercooler design.
The 6th generation was used only very briefly as teams saw little advantage in switching to a new body style. Teams were actually lobbying extensively to switch over to the Corolla. The Corolla, in driver's opinions, was a superior car for rally in that it was lighter and had a better view of the road. With the Corolla, Toyota did not see the success that it did with the Celica and ultimately pulled out of WRC in 1998 in favor of F1.
Based off of the 6th Generation Celica body shell the Pikes Peak Celica has very little in common with a production Celica. From a 4 cylinder Toyota/TRD Racing engine to a carbon composite body shell, X-Trac transmission, to 4wd...the Celica is probably one of the most expensive, technologically advanced Celicas ever built. Although GT-4s were released overseas it is interesting that the Pikes Peak Celica isn't based off of the GT-4 design (note the hood differences). My speculation is that this is either due to an aerodynamic advantage or an engine design that eliminates the top mount intercooler. With an estimated 800HP on tap and a huge wing that keep the Celica firmly planted on the dirt, Rod Millen made several record shattering runs, including setting a Pikes Peak record that is still standing. Unfortunately, as Toyota moved out of WRC the Pikes Peak Celica was dropped in place of a Tacoma body shell. Toyota finally dropped the funding of the Pikes Peak Hill Climb all together in 2001.
Introduced in 2002 the NHRA Celica is Toyota's venture into drag racing. Competing in the funny car class this car really has very little similar to a Celica besides the paint scheme. If you do consider this a "Celica" however this may be the most powerful Celica ever built. The supercharged, nitro-burning, tire-spinning stats put it at a whopping 6000+ HP. The NHRA Celica is capable of reaching speeds over 320mph with quarter mile times less than 5 seconds.


text:
News, Training
Woman Kicked Paramedic in Face as He Treated Her
Drunken barmaid Mandy Bryan kicked a paramedic in the face — as he tried to check her blood pressure.
The trainee teaching assistant had been found slumped in the toilet of a Stafford pub.
But the paramedics suspected Bryan was pretending to be unconscious and was taken to the pub's living quarters.
The defendant was then sick before she kicked paramedic David Jenkinson hard on the right side of the face.
After that, she pretended to be asleep, and later got up and made her own way out of the pub. Mr Jenkinson was treated in hospital for a suspected hairline fracture of the cheek.
Stephen Bailey, mitigating, said Bryan was training to be a teaching assistant and was hoping to be offered a job, if she avoided custody.
Bryan, aged 28, of Booth Street, Chesterton, who admitted assault, was yesterday handed a fourmonth prison sentence, suspended for 18 months, and ordered to pay £350 compensation. Judge Paul Glenn told her: I take a serious view of this case. "The victim is a paramedic simply trying to do his job and help you.
"He was upset because he was offering assistance to a patient. "You got yourself in to this state by drinking an obscene mixture of alcohol.
"You were pretending to be more ill than you were.
I would normally send someone to prison for this — your previous good character and guilty plea is just about enough to suspend it, but it"s been a close run thing.
A Push for Push Dose Epinephrine
Twenty-First Century Patient Assessment
Building a System of Resuscitation- The Advanced Medical Transport Story


A communication protocol is a system of rules that allow two or more entities of a communications system to transmit information via any kind of variation of a physical quantity. These are the rules or standard that defines the syntax, semantics and synchronization of communication and possible error recovery methods. Protocols may be implemented by hardware, software, or a combination of both.
The book HTTP2 Explained describes the protocol HTTP/2 at a technical and protocol level. Background, the protocol, the implementations and the future.
With HTTP Succinctly, you'll learn all about something you use on a daily basis.
You'll then dive into performance characteristics of technologies such as HTTP 2.0, client-side network scripting with XHR, real-time streaming with SSE and WebSocket, and P2P communication with WebRTC.


text:
Alcohol, sometimes referred to by the chemical name ethanol, is a depressant drug that is the active ingredient in drinks such as beer, wine, and distilled spirits (hard liquor). It is one of the oldest and most commonly consumed recreational drugs, causing the characteristic effects of alcohol intoxication ("drunkenness"). Among other effects, alcohol produces happiness and euphoria, decreased anxiety, increased sociability, sedation, impairment of cognitive, memory, motor, and sensory function, and generalized depression of central nervous system (CNS) function. Ethanol is only one of several types of alcohol, but it is the only type of alcohol that is found in alcoholic beverages or commonly used for recreational purposes; other alcohols such as methanol and isopropyl alcohol are significantly more toxic.  A mild, brief exposure to isopropanol, being only moderately more toxic than ethanol, is unlikely to cause any serious harm. Methanol, being profoundly more toxic than ethanol, is lethal in quantities as small as 10–15 milliliters (2–3 teaspoons).

Alcohol has a variety of short-term and long-term adverse effects. Short-term adverse effects include generalized impairment of neurocognitive function, dizziness, nausea, vomiting, and hangover-like symptoms. Alcohol is addictive to humans, and can result in alcohol use disorder, dependence and withdrawal. It can have a variety of long-term adverse effects on health, such as liver and brain damage, and its consumption can cause cancer. The adverse effects of alcohol on health are most important when it is used in excessive quantities or with heavy frequency. However, some of them, such as increased risk of certain cancers, may occur even with light or moderate alcohol consumption. In high amounts, alcohol may cause loss of consciousness or, in severe cases, death.

Alcohol works in the brain primarily by increasing the effects of γ-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in the brain; by facilitating GABA's actions, alcohol suppresses the activity of the CNS. The substance also directly affects a number of other neurotransmitter systems including those of glutamate, glycine, acetylcholine, and serotonin. The pleasurable effects of alcohol ingestion are the result of increased levels of dopamine and endogenous opioids in the reward pathways of the brain. Alcohol also has toxic and unpleasant actions in the body, many of which are mediated by its byproduct acetaldehyde.

Alcohol has been produced and consumed by humans for its psychoactive effects for almost 10,000 years. Drinking alcohol is generally socially acceptable and is legal in most countries, unlike with many other recreational substances. However, there are often restrictions on alcohol sale and use, for instance a minimum age for drinking and laws against public drinking and drinking and driving. Alcohol has considerable societal and cultural significance and has important social roles in much of the world. Drinking establishments, such as bars and nightclubs, revolve primarily around the sale and consumption of alcoholic beverages, and parties, festivals, and social gatherings commonly involve alcohol consumption. Alcohol is unique in that it is the only drug that damages others more than the user. It is related to various societal problems, including drunk driving, accidental injuries, sexual assaults, domestic abuse, and violent crime. Alcohol remains illegal for sale and consumption in a number of countries, mainly in the Middle East. While some religions, including Islam, prohibit alcohol consumption, other religions, such as Christianity and Shinto, utilize alcohol in sacrament and libation.

Use and effects

Ethanol is typically consumed as a recreational substance by mouth in the form of alcoholic beverages such as beer, wine, and spirits. It is commonly used in social settings due to its capacity to enhance sociability.

The amount of ethanol in the body is typically quantified by blood alcohol content (BAC); weight of ethanol per unit volume of blood. Small doses of ethanol, in general, are stimulant-like and produce euphoria and relaxation; people experiencing these symptoms tend to become talkative and less inhibited, and may exhibit poor judgement. At higher dosages (BAC > 1 gram/liter), ethanol acts as a central nervous system (CNS) depressant, producing at progressively higher dosages, impaired sensory and motor function, slowed cognition, stupefaction, unconsciousness, and possible death. Ethanol is commonly consumed as a recreational substance, especially while socializing, due to its psychoactive effects.

Standard drink
There is no single standard, but a standard drink of 10 g alcohol (12.7 millilitres), which is used in the World Health Organization (WHO) Alcohol Use Disorders Identification Test (AUDIT)'s questionnaire form example, have been adopted by more countries than any other amount.

Toxicity

Alcohol has a variety of short-term and long-term adverse effects. It also has reinforcement-related adverse effects, including addiction, dependence, and withdrawal.

Social harm

Alcohol causes a plethora of detrimental effects in society. It is highly associated with drinking in public, passive drinking, drunk dialing, drunk driving, sexual risk-taking or drug facilitated sexual assault (especially with caffeinated alcoholic drinks), and both violent and non-violent crime. About one-third of arrests in the United States involve alcohol misuse. Many emergency room visits also involve alcohol use. As many as 15% of employees show problematic alcohol-related behaviors in the workplace, such as drinking before going to work or even drinking on the job. Heavy drinking is associated with vulnerability to injury, marital discord, and domestic violence. Alcohol use is directly related to considerable morbidity and mortality, for instance due to overdose and alcohol-related health problems.

Alcohol-related crimes

Automobile accidents

A 2002 study found 41% of people fatally injured in traffic accidents were in alcohol-related crashes. Misuse of alcohol is associated with more than 40% of deaths that occur in automobile accidents every year. The risk of a fatal car accident increases exponentially with the level of alcohol in the driver's blood. Most drunk driving laws in the U.S. governing the acceptable levels in the blood while driving or operating heavy machinery set typical upper limits of legal BAC at 0.08%.

Sexual assault

Alcohol is often used to facilitate sexual assault or rape. Over 50% of reported rapes involve alcohol. It is the most commonly used date rape drug.

Violent crime

Over 40% of all assaults and 40 to 50% of all murders involve alcohol. More than 43% of violent encounters with police involve alcohol. Alcohol is implicated in more than two-thirds of cases of intimate partner violence. In 2002, it was estimated that 1 million violent crimes in the U.S. were related to alcohol use. Alcohol is more commonly associated with both violent and non-violent crime than are drugs like marijuana.

Health consequences

Alcohol use disorder is a major problem and many health problems as well as death can result from excessive alcohol use. Alcohol dependence is linked to a lifespan that is reduced by about 12 years relative to the average person. In 2004, it was estimated that 4% of deaths worldwide were attributable to alcohol use. Deaths from alcohol are split about evenly between acute causes (e.g., overdose, accidents) and chronic conditions. The leading chronic alcohol-related condition associated with death is alcoholic liver disease. Alcohol dependence is also associated with cognitive impairment and organic brain damage. Some researchers have found that even one alcoholic drink a day increases an individual's risk of health problems by 0.4%.

Adverse effects

Short-term effects

Central nervous system impairment
Alcohol causes generalized CNS depression, is a positive allosteric GABAA modulator and is associated and related with cognitive, memory, motor, and sensory impairment. It slows and impairs cognition and reaction time and the cognitive skills, impairs judgement, interferes with motor function resulting in motor incoordination, loss of balance, confusion, sedation, numbness and slurred speech, impairs memory formation, and causes sensory impairment. At high concentrations, it can induce amnesia, analgesia, spins, stupor, and unconsciousness as result of high levels of ethanol in blood.

At very high concentrations, alcohol can cause anterograde amnesia, markedly decreased heart rate, pulmonary aspiration, positional alcohol nystagmus, respiratory depression, shock, coma and death can result due to profound suppression of CNS function alcohol overdose and can finish in consequent dysautonomia.

Gastrointestinal effects

Alcohol can cause nausea and vomiting in sufficiently high amounts (varying by person).

Alcohol stimulates gastric juice production, even when food is not present, and as a result, its consumption stimulates acidic secretions normally intended to digest protein molecules. Consequently, the excess acidity may harm the inner lining of the stomach. The stomach lining is normally protected by a mucosal layer that prevents the stomach from, essentially, digesting itself. However, in patients who have a peptic ulcer disease (PUD), this mucosal layer is broken down. PUD is commonly associated with the bacteria Helicobacter pylori, which secretes a toxin that weakens the mucosal wall, allowing acid and protein enzymes to penetrate the weakened barrier. Because alcohol stimulates the stomach to secrete acid, a person with PUD should avoid drinking alcohol on an empty stomach. Drinking alcohol causes more acid release, which further damages the already-weakened stomach wall. Complications of this disease could include a burning pain in the abdomen, bloating and in severe cases, the presence of dark black stools indicate internal bleeding. A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation.

Ingestion of alcohol can initiate systemic pro-inflammatory changes through two intestinal routes: (1) altering intestinal microbiota composition (dysbiosis), which increases lipopolysaccharide (LPS) release, and (2) degrading intestinal mucosal barrier integrity – thus allowing LPS to enter the circulatory system. The major portion of the blood supply to the liver is provided by the portal vein. Therefore, while the liver is continuously fed nutrients from the intestine, it is also exposed to any bacteria and/or bacterial derivatives that breach the intestinal mucosal barrier. Consequently, LPS levels increase in the portal vein, liver and systemic circulation after alcohol intake. Immune cells in the liver respond to LPS with the production of reactive oxygen species, leukotrienes, chemokines and cytokines. These factors promote tissue inflammation and contribute to organ pathology.

Allergic-like reactions

Ethanol-containing beverages can cause alcohol flush reactions, exacerbations of rhinitis and, more seriously and commonly, bronchoconstriction in patients with a history of asthma, and in some cases, urticarial skin eruptions, and systemic dermatitis.  Such reactions can occur within 1–60 minutes of ethanol ingestion, and may be caused by:
 genetic abnormalities in the metabolism of ethanol, which can cause the ethanol metabolite, acetaldehyde, to accumulate in tissues and trigger the release of histamine, or
 true allergy reactions to allergens occurring naturally in, or contaminating, alcoholic beverages (particularly wine and beer), and
 other unknown causes.

Long-term effects

Prolonged heavy consumption of alcohol can cause significant permanent damage to the brain and other organs, resulting in dysfunction or death.

Brain damage

Alcohol can cause brain damage, Wernicke's encephalopathy and Alcoholic Korsakoff syndrome which frequently occur simultaneously, known as Wernicke–Korsakoff syndrome. Lesions, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss.

Liver damage

During the metabolism of alcohol via the respective dehydrogenases, nicotinamide adenine dinucleotide (NAD) is converted into reduced NAD. Normally, NAD is used to metabolize fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcohol use disorder) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis.

Birth defects

Ethanol is classified as a teratogen. According to the U.S. Centers for Disease Control and Prevention (CDC), alcohol consumption by women who are not using birth control increases the risk of fetal alcohol syndrome. The CDC currently recommends complete abstinence from alcoholic beverages for women of child-bearing age who are pregnant, trying to become pregnant, or are sexually active and not using birth control.

Cancer
The International Agency for Research on Cancer lists ethanol in alcoholic beverages as a Group 1 carcinogen in humans and argues that "There is sufficient evidence and research showing the carcinogenicity of acetaldehyde (the major metabolite of ethanol) which is excreted by the liver enzyme when one drinks alcohol."

 Other effects
Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of triglycerides.

 Reinforcement disorders

 Addiction, dependence and withdrawal

Alcohol addiction is termed alcohol use disorder. Two or more consecutive alcohol-free days a week have been recommended to improve health and break dependence.

Discontinuation of alcohol after extended heavy use and associated tolerance development (resulting in dependence) can result in withdrawal. Alcohol withdrawal can cause confusion, paranoia, anxiety, insomnia, agitation, tremors, fever, nausea, vomiting, autonomic dysfunction, seizures, and hallucinations. In severe cases, death can result. Delirium tremens is a condition that requires people with a long history of heavy drinking to undertake an alcohol detoxification regimen.

 Overdose

Death from ethanol consumption is possible when blood alcohol levels reach 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3–0.4%.

The oral median lethal dose (LD50) of ethanol in rats is 5,628 mg/kg. Directly translated to human beings, this would mean that if a person who weighs  drank a  glass of pure ethanol, they would theoretically have a 50% risk of dying. Symptoms of ethanol overdose may include nausea, vomiting, CNS depression, coma, acute respiratory failure, or death.

 Interactions

Alcohol can intensify the sedation caused by other CNS depressants such as barbiturates, benzodiazepines, opioids, nonbenzodiazepines/Z-drugs (such as zolpidem and zopiclone), antipsychotics, sedative antihistamines, and certain antidepressants. It interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance. Ethanol enhances the bioavailability of methylphenidate (elevated plasma dexmethylphenidate). In combination with cannabis, ethanol increases plasma tetrahydrocannabinol levels, which suggests that ethanol may increase the absorption of tetrahydrocannabinol.

 Disulfiram-like drugs

 Disulfiram
Disulfiram inhibits the enzyme acetaldehyde dehydrogenase, which in turn results in buildup of acetaldehyde, a toxic metabolite of ethanol with unpleasant effects. The medication or drug is commonly used to treat alcohol use disorder, and results in immediate hangover-like symptoms upon consumption of alcohol, this effect is widely known as disulfiram effect.

 Metronidazole
One of the most important drug/food interactions is between alcohol and metronidazole.

Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function. Metronidazole is usually given to people who have diarrhea caused by Clostridium difficile bacteria. C. difficile is one of the most common microorganisms that cause diarrhea and can lead to colon inflammation and more severely, death.

Patients who are taking metronidazole are sometimes advised to avoid alcohol, even after 1 hour following the last dose. Although older data suggested a possible disulfiram-like effect of metronidazole, newer data has challenged this and suggests it does not actually have this effect.

 Methanol and ethylene glycol

The rate-limiting steps for the elimination of ethanol are in common with certain other substances. As a result, the blood alcohol concentration can be used to modify the rate of metabolism of methanol and ethylene glycol. Methanol itself is not highly toxic, but its metabolites formaldehyde and formic acid are; therefore, to reduce the rate of production and concentration of these harmful metabolites, ethanol can be ingested. Ethylene glycol poisoning can be treated in the same way.

 Pharmacology
 Dynamics

The precise mechanism of action of ethanol has proven elusive and remains not fully understood. Identifying molecular targets for ethanol has proven unusually difficult, in large part due to its unique biochemical properties. Specifically, ethanol is a very low molecular weight compound and is of exceptionally low potency in its actions, causing effects only at very high (millimolar (mM)) concentrations. For these reasons, unlike with most drugs, it has not yet been possible to employ traditional biochemical techniques to directly assess the binding of ethanol to receptors or ion channels. Instead, researchers have had to rely on functional studies to elucidate the actions of ethanol. Moreover, although it has been established that ethanol modulates ion channels to mediate its effects, ion channels are complex proteins, and their interactions and functions are complicated by diverse subunit compositions and regulation by conserved cellular signals (e.g. signaling lipids).

Much progress has been made in understanding the pharmacodynamics of ethanol over the last few decades. While no binding sites have been identified and established unambiguously for ethanol at present, it appears that it affects ion channels, in particular ligand-gated ion channels, to mediate its effects in the CNS. Ethanol has specifically been found in functional assays to enhance or inhibit the activity of a variety of ion channels, including the GABAA receptor, the ionotropic glutamate AMPA, kainate, and NMDA receptors, the glycine receptor, the nicotinic acetylcholine receptors, the serotonin 5-HT3 receptor, voltage-gated calcium channels, and BK channels, among others. However, many of these actions have been found to occur only at very high concentrations that may not be pharmacologically significant at recreational doses of ethanol, and it is unclear how or to what extent each of the individual actions is involved in the effects of ethanol. In any case, ethanol has long shown a similarity in its effects to positive allosteric modulators of the GABAA receptor like benzodiazepines, barbiturates, and various general anesthetics. Indeed, ethanol has been found to enhance GABAA receptor-mediated currents in functional assays. In accordance, it is theorized and widely believed that the primary mechanism of action is as a GABAA receptor positive allosteric modulator. However, the diverse actions of ethanol on other ion channels may be and indeed likely are involved in its effects as well.

In 2007, it was discovered that ethanol potentiates extrasynaptic δ subunit-containing GABAA receptors at behaviorally relevant (as low as 3 mM) concentrations. This is in contrast to previous functional assays of ethanol on γ subunit-containing GABAA receptors, which it enhances only at far higher concentrations (> 100 mM) that are in excess of recreational concentrations (up to 50 mM). Ro15-4513, a close analogue of the benzodiazepine antagonist flumazenil (Ro15-1788), has been found to bind to the same site as ethanol and to competitively displace it in a saturable manner. In addition, Ro15-4513 blocked the enhancement of δ subunit-containing GABAA receptor currents by ethanol in vitro. In accordance, the drug has been found to reverse many of the behavioral effects of low-to-moderate doses of ethanol in rodents, including its effects on anxiety, memory, motor behavior, and self-administration. Taken together, these findings suggest a binding site for ethanol on subpopulations of the GABAA receptor with specific subunit compositions via which it interacts with and potentiates the receptor.

A 2019 study showed the accumulation of an unnatural lipid phosphatidylethanol (PEth) competes with PIP2 agonist sites on lipid-gated ion channels. This presents a novel indirect mechanism and suggests that a metabolite, not the ethanol itself, can affect the primary targets of ethanol intoxication. Many of the primary targets of ethanol are known to bind PIP2 including GABAA receptors, but the role of PEth will need to be investigated for each of the primary targets.

 Rewarding and reinforcing actions
The reinforcing effects of alcohol consumption are mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P-4502E1 in the brain. Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic dopamine system.

Ethanol's rewarding and reinforcing (i.e., addictive) properties are mediated through its effects on dopamine neurons in the mesolimbic reward pathway, which connects the ventral tegmental area to the nucleus accumbens (NAcc). One of ethanol's primary effects is the allosteric inhibition of NMDA receptors and facilitation of GABAA receptors (e.g., enhanced GABAA receptor-mediated chloride flux through allosteric regulation of the receptor). At high doses, ethanol inhibits most ligand-gated ion channels and voltage-gated ion channels in neurons as well.

With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors. The activation of these receptors triggers postsynaptic internal signaling events through protein kinase A, which ultimately phosphorylate cAMP response element binding protein (CREB), inducing CREB-mediated changes in gene expression.

With chronic alcohol intake, consumption of ethanol similarly induces CREB phosphorylation through the D1 receptor pathway, but it also alters NMDA receptor function through phosphorylation mechanisms; an adaptive downregulation of the D1 receptor pathway and CREB function occurs as well. Chronic consumption is also associated with an effect on CREB phosphorylation and function via postsynaptic NMDA receptor signaling cascades through a MAPK/ERK pathway and CAMK-mediated pathway. These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the , where ΔFosB is the "master control protein" that, when overexpressed in the NAcc, is necessary and sufficient for the development and maintenance of an addictive state (i.e., its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption).

 Relationship between concentrations and effects

Recreational concentrations of ethanol are typically in the range of 1 to 50 mM. Very low concentrations of 1 to 2 mM ethanol produce zero or undetectable effects except in alcohol-naive individuals. Slightly higher levels of 5 to 10 mM, which are associated with light social drinking, produce measurable effects including changes in visual acuity, decreased anxiety, and modest behavioral disinhibition. Further higher levels of 15 to 20 mM result in a degree of sedation and motor incoordination that is contraindicated with the operation of motor vehicles. In jurisdictions in the U.S., maximum blood alcohol levels for legal driving are about 17 to 22 mM. In the upper range of recreational ethanol concentrations of 20 to 50 mM, depression of the central nervous system is more marked, with effects including complete drunkenness, profound sedation, amnesia, emesis, hypnosis, and eventually unconsciousness. Levels of ethanol above 50 mM are not typically experienced by normal individuals and hence are not usually physiologically relevant; however, such levels – ranging from 50 to 100 mM – may be experienced by alcoholics with high tolerance to ethanol. Concentrations above this range, specifically in the range of 100 to 200 mM, would cause death in all people except alcoholics.

 List of known actions in the central nervous system
Ethanol has been reported to possess the following actions in functional assays at varying concentrations:

 GABAA receptor positive allosteric modulator (primarily of δ subunit-containing receptors)
 NMDA receptor negative allosteric modulator
 Decreased levels of nitric oxide in brain medulla
 Increased levels of dopamine and endogenous opioids in the mesolimbic pathway, secondary to other actions
 AMPA receptor negative allosteric modulator
 Kainate receptor negative allosteric modulator
 Glycine receptor positive allosteric modulator
 Serotonin receptor positive allosteric modulator
 Opioid receptor endogenous positive allosteric modulator
 Muscarinic acetylcholine receptor positive allosteric modulator.
 Nicotinic acetylcholine receptor positive allosteric modulator
 5-HT3 receptor positive allosteric modulator
 Glycine reuptake inhibitor
 Adenosine reuptake inhibitor
 Dopamine reuptake inhibitor
 L-type calcium channel blocker
 GIRK channel opener

Some of the actions of ethanol on ligand-gated ion channels, specifically the nicotinic acetylcholine receptors and the glycine receptor, are dose-dependent, with potentiation or inhibition occurring dependent on ethanol concentration. This seems to be because the effects of ethanol on these channels are a summation of positive and negative allosteric modulatory actions.

 Kinetics
 Absorption
Ethanol can be taken orally, by inhalation, rectally, or by injection (e.g., intravenous), though it is typically ingested simply via oral administration. The oral bioavailability of ethanol is around 80% or more. In fasting volunteers, blood levels of ethanol increase proportionally with the dose of ethanol administered. Blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution.

Onset
Peak circulating levels of ethanol are usually reached within a range of 30 to 90 minutes of ingestion, with an average of 45 to 60 minutes. People who have fasted overnight have been found to reach peak ethanol concentrations more rapidly, at within 30 minutes of ingestion.

The onset varies depends on the type of alcoholic drink:
 Vodka/tonic: 36 ± 10 minutes
 Wine: 54 ± 14 minutes
 Beer: 62 ± 23 minutes

Also, carbonated alcoholic drinks seem to have a shorter onset compare to flat drinks in the same volume. One theory is that carbon dioxide in the bubbles somehow speeds the flow of alcohol into the intestines.

Food in the gastrointestinal system and hence gastric emptying is the most important factor that influences the absorption of orally ingested ethanol. The absorption of ethanol is much more rapid on an empty stomach than with a full one. The delay in ethanol absorption caused by food is similar regardless of whether food is consumed just before, at the same time, or just after ingestion of ethanol. The type of food, whether fat, carbohydrates, or protein, also is of little importance. Not only does food slow the absorption of ethanol, but it also reduces the bioavailability of ethanol, resulting in lower circulating concentrations.

 Distribution
Upon ingestion, ethanol is rapidly distributed throughout the body. It is distributed most rapidly to tissues with the greatest blood supply. As such, ethanol primarily affects the brain, liver, and kidneys. Other tissues with lower circulation, such as bone, require more time for ethanol to distribute into. Ethanol crosses biological membranes and the blood–brain barrier easily, through a simple process of passive diffusion. The volume of distribution of ethanol is around . It is only weakly or not at all plasma protein bound.

 Metabolism

Approximately 90% of the metabolism of ethanol occurs in the liver. This occurs predominantly via the enzyme alcohol dehydrogenase, which transforms ethanol into its metabolite acetaldehyde (ethanal). Acetaldehyde is subsequently metabolized by the enzyme aldehyde dehydrogenase into acetate (ethanoate), which in turn is broken down into carbon dioxide and water. Acetate also combines with coenzyme A to form acetyl-CoA, and hence may participate in metabolic pathways. Alcohol dehydrogenase and aldehyde dehydrogenase are present at their highest concentrations in the liver, but are widely expressed throughout the body, and alcohol dehydrogenase may also be present in the stomach and small intestine. Aside from alcohol dehydrogenase, the microsomal ethanol-oxidizing system (MEOS), specifically mediated by the cytochrome P450 enzyme CYP2E1, is the other major route of ethanol metabolism. CYP2E1 is inducible by ethanol, so while alcohol dehydrogenase handles acute or low concentrations of ethanol, MEOS is predominant with higher concentrations or with repeated/chronic use. A small amount of ethanol undergoes conjugation to form ethyl glucuronide and ethyl sulfate. There may also be another metabolic pathway that metabolizes as much as 25 to 35% of ethanol at typical concentrations.

At even low physiological concentrations, ethanol completely saturates alcohol dehydrogenase. This is because ethanol has high affinity for the enzyme and very high concentrations of ethanol occur when it is used as a recreational substance. For this reason, the metabolism of ethanol follows zero-order kinetics at typical physiological concentrations. That is, ethanol does not have an elimination half-life (i.e., is not metabolized at an exponential rate), and instead, is eliminated from the circulation at a constant rate. The mean elimination rates for ethanol are 15 mg/dL per hour for men and 18 mg/dL per hour for women, with a range of 10 to 34 mg/dL per hour. At very high concentrations, such as in overdose, it has been found that the rate of elimination of ethanol is increased. In addition, ethanol metabolism follows first-order kinetics at very high concentrations, with an elimination half-life of about 4 or 4.5 hours (which implies a clearance rate of approximately 6 L/hour/70 kg). This seems to be because other processes, such as the MEOS/CYP2E1, also become involved in the metabolism of ethanol at higher concentrations. However, the MEOS/CYP2E1 alone does not appear sufficient to fully explain the increase in ethanol metabolism rate.

Some individuals have less effective forms of one or both of the metabolizing enzymes of ethanol, and can experience more marked symptoms from ethanol consumption than others. However, those having acquired alcohol tolerance have a greater quantity of these enzymes, and metabolize ethanol more rapidly.

 Elimination
Ethanol is mainly eliminated from the body via metabolism into carbon dioxide and water. Around 5 to 10% of ethanol that is ingested is eliminated unchanged in urine, breath, and sweat. Transdermal alcohol that diffuses through the skin as insensible perspiration or is exuded as sweat (sensible perspiration) can be detected using wearable sensor technology such as SCRAM ankle bracelet or the more discreet ION Wearable. Ethanol or its metabolites may be detectable in urine for up to 96 hours (3–5 days) after ingestion.

 Chemistry

Ethanol is also known chemically as alcohol, ethyl alcohol, or drinking alcohol. It is a simple alcohol with a molecular formula of C2H6O and a molecular weight of 46.0684 g/mol. The molecular formula of ethanol may also be written as CH3−CH2−OH or as C2H5−OH. The latter can also be thought of as an ethyl group linked to a hydroxyl (alcohol) group and can be abbreviated as EtOH. Ethanol is a volatile, flammable, colorless liquid with a slight characteristic odor. Aside from its use as a psychoactive and recreational substance, ethanol is also commonly used as an antiseptic and disinfectant, a chemical and medicinal solvent, and a fuel.

 Production
Ethanol is produced naturally as a byproduct of the metabolic processes of yeast and hence is present in any yeast habitat, including even endogenously in humans, but it does not cause raised blood alcohol content as seen in the rare medical condition auto-brewery syndrome (ABS). It is manufactured through hydration of ethylene or by brewing via fermentation of sugars with yeast (most commonly Saccharomyces cerevisiae). The sugars are commonly obtained from sources like steeped cereal grains (e.g., barley), grape juice, and sugarcane products (e.g., molasses, sugarcane juice). Ethanol–water mixture which can be further purified via distillation.

 Analogues

Ethanol has a variety of analogues, many of which have similar actions and effects. Methanol (methyl alcohol) and isopropyl alcohol (also called rubbing alcohol) are both toxic, and thus unsafe for human consumption. Methanol is the most toxic alcohol; the toxicity of isopropyl alcohol lies between that of ethanol and methanol, and is about twice that of ethanol. In general, higher alcohols are less toxic. n-Butanol is reported to produce similar effects to those of ethanol and relatively low toxicity (one-sixth of that of ethanol in one rat study). However, its vapors can produce eye irritation and inhalation can cause pulmonary edema. Acetone (propanone) is a ketone rather than an alcohol, and is reported to produce similar toxic effects; it can be extremely damaging to the cornea.

The tertiary alcohol tert-amyl alcohol (TAA), also known as 2-methylbutan-2-ol (2M2B), has a history of use as a hypnotic and anesthetic, as do other tertiary alcohols such as methylpentynol, ethchlorvynol, and chloralodol. Unlike primary alcohols like ethanol, these tertiary alcohols cannot be oxidized into aldehyde or carboxylic acid metabolites, which are often toxic, and for this reason, these compounds are safer in comparison. Other relatives of ethanol with similar effects include chloral hydrate, paraldehyde, and many volatile and inhalational anesthetics (e.g., chloroform, diethyl ether, and isoflurane).

 History

Alcohol was brewed as early as 7,000 to 6,650 BCE in northern China. The earliest evidence of winemaking was dated at 6,000 to 5,800 BCE in Georgia in the South Caucasus. Beer was likely brewed from barley as early as the 6th century BCE (600–500 BCE) in Egypt. Pliny the Elder wrote about the golden age'' of winemaking in Rome, the 2nd century BCE (200–100 BCE), when vineyards were planted.

Society and culture

Legal status

Alcohol consumption is fully legal and available in most countries of the world. Home made alcoholic beverages with low alcohol content like wine, and beer is also legal in most countries, but distilling moonshine outside a registered distillery remains illegal in most of them.

Some majority-Muslim countries, such as Saudi Arabia, Kuwait, Pakistan, Iran and Libya prohibit the production, sale, and consumption of alcoholic beverages because they are forbidden by Islam. Also, laws banning alcohol consumption are found in  some Indian states as well as some Native American reservations in the U.S.

In addition, there are regulations on alcohol sales and use in many countries throughout the world. For instance, some countries have a minimum legal age to purchase or consume alcoholic beverages.  Also, some countries have bans on public intoxication. Drinking while driving or intoxicated driving is frequently outlawed and it may be illegal to have an open container of alcohol or liquor bottle in an automobile, bus or aircraft.

See also
 Binge drinking
 Comparison of psychoactive alcohols in alcoholic drinks
 Holiday heart syndrome

References

Further reading
 The National Institute on Alcohol Abuse and Alcoholism maintains a database of alcohol-related health effects. ETOH Archival Database (1972–2003) Alcohol and Alcohol Problems Science Database.

External links
 ChEBI – biology related
 Kyoto Encyclopedia of Genes and Genomes signal transduction pathway: KEGG – human alcohol addiction

5-HT3 agonists
AMPA receptor antagonists
Adenosine reuptake inhibitors
Alcohol dehydrogenase inhibitors
Alcohol
Alcohols
Analgesics
Anxiolytics
Calcium channel blockers
Drinking culture
Drug culture
Drugs acting on the nervous system
Ethanol
Euphoriants
GABAA receptor positive allosteric modulators
General anesthetics
Glycine reuptake inhibitors
Hepatotoxins
Hypnotics
IARC Group 1 carcinogens
Kainate receptor antagonists
NMDA receptor antagonists
Neurotoxins
Nicotinic agonists
Psychoactive drugs
Sedatives
Teratogens


text:
Q: Ruby gem to generate GIF CSS sprites from PNGs? Is there a Ruby gem that can generate CSS sprites from PNG images by combining them into a GIF?
I am looking for one that supports command line. I found several but they either work only with Rails or can only produce PNG sprites, never gifs.

A: Another big caveat with GIF is that you're limited to a 256-color palette, which is often fine for a single image but could be problematic if your sprites vary widely in palette. Regardless...
css_sprite (the first result for this gem search) looks like your best bet.
You probably found it on your own and disregarded it because it appears to depend on Rails. However, peeking at the code shows that in fact it doesn't. Running it as specified should work as long as your configuration file is specified.*
*It looks like the css_sprite:build Rake task might break without Rails (because it doesn't require lib/automatic.rb, which "fakes" Rails.root) but using rake css_sprite:start should work fine.

redpajama_set_name: RedPajamaStackExchange


text:
Kermode junior boys took silver in the zone final series against the Rainmakers.
Caledonia Kermodes take second in junior boys zones
Terrace boys kept their usual close score against the undefeated Prince Rupert Rainmakers
Jackie Lieuwen
Feb. 10, 2018 12:00 a.m.
The Terrace junior boys played two close games but lost zone final against the Charles Hayes Rainmakers this weekend.
The first game saw Caledonia Kermode Brody McKay land a beautiful three-point buzzer beater to launch the boys into overtime 41-41.
And though Terrace's Cole Ouellet managed to score a basket, the Charles Hayes squad netted 14 points overall to take the victory 55-43.
The second game followed a similar pattern, with Charles Hayes leading but only by a margin for nearly the whole match.
In the final two minutes, the Kermodes started building some momentum, scoring two baskets, and called a time out with just over a minute left, standing behind by a narrow 32-35.
But Prince Rupert hooped a three to kill their momentum, and then notched two penalty shots to take the win 40-32.
Kermode coach Matt Lowndes said he thought the Terrace boys competed well.
"Charles Hayes is a good basketball team," he said. "Their defence is tough, they don't give up too many baskets.
"Both games could have gone either way."
And that's been the trend against the Rainmakers all season, he added, noting that while the Kermodes lost all three season games against them, they always give them a solid run for their money.
Prince Rupert coach Kevin Sawka said much the same.
"We've had a really good record this year," he said of the Rainmakers, noting that they've had an undefeated season and played a number of strong games with community teams and their senior boys second string.
Last weekend's zone final was good, close competition, he added.
"I was really proud of how the guys (Rainmakers) played," he said, adding that the team has faced a bit of an emotional roller coaster this season.
"We've got a kid on our team that's not with us this weekend, he's got some health stuff going on… The guys are dedicating the zone championship to him," said Sawka.
"And I want to give credit to Terrace… they've worked really hard to improve this year," he said, noting that their shooting is pretty consistent, particularly with Brody McKay and James Gagnon.
"And I would say Cole Outlet, his length and size, I would say is the bigger factor… he forces our defence to collapse, he draws a lot of attention, so even if he doesn't affect the score sheet a lot, (it's) all the other stuff that he's doing — he's changing shots, he's getting rebounds, and collapsing the defence.
Sawka says from as far back as when he played in 2002, Terrace always seems to play better at home.
"If there was ever a team that had a home court advantage, this is them. They always play better at home," he said, adding that it's not the refereeing that makes the difference.
Terrace's Brody McKay and Cole Ouellet earned All-Stars, along with Rupert's Brendan Eshom and Caden Pagens.
James Gagnon was named top defensive player and Rupert's Tyler Jones took the overall MVP.
McKay and Gagnon said they were pleased with their improvement this year.
"It was a lot better than last year," said McKay.
Gagnon added, "we played good, in our first game we had a lot of turnovers, but we made up for it on defence."
And that improvement came specifically in their coverage of MVP Tyler Jones.
"He used to draw 30 points a game last year," said McKay, "but I think the most he's ever scored against us this year is 12."
Gagnon has guarded Tyler all year, and said it's fun, but tough.
"It's pretty hard, he's really fast… (but) it's always fun playing him," Gagnon said.
Veteran Blue Jays broadcaster Jerry Howarth to retire
Top-ranked Mariners men win more matches


text:
Louisa Fraser1
F, #247381, d. 23 September 1843
Last Edited=14 Oct 2007
Louisa Fraser married Thomas Grierson, son of Colonel James Grierson and Katherine McBurnie, on 7 January 1792 at New Abbey, Kirkcudbrightshire, ScotlandG.1 She died on 23 September 1843 at Helensburgh, ScotlandG.1
From 7 January 1792, her married name became Grierson.1
Child of Louisa Fraser and Thomas Grierson
Louisa Grierson+1 b. 6 Jun 1794, d. 29 Feb 1864
[S2249] David Alan, 1960 (aka Lyon) Grierson, "re: Grierson Family," e-mail message to Darryl Roger Lundy, 16 April 2007. Hereinafter cited as "re: Grierson Family."
Louisa Grierson1
F, #247382, b. 6 June 1794, d. 29 February 1864
Louisa Grierson was born on 6 June 1794 at New Abbey, Kirkcudbrightshire, ScotlandG.1 She was the daughter of Thomas Grierson and Louisa Fraser.1 She married John Litt on 7 July 1828 at Glasgow, Lanarkshire, ScotlandG.1 She died on 29 February 1864 at age 69 at Bath, Somerset, EnglandG.1
From 7 July 1828, her married name became Litt.1
Children of Louisa Grierson and John Litt
Louisa Dorothea Litt1 b. 17 Sep 1829
Helen Maxwell Litt1 b. Aug 1831
Helen Theresa Litt+1 b. 10 Sep 1833
Harriett Eliza Litt1 b. 6 Aug 1835
Frances Litt1 b. May 1837
Robert Needham, 3rd Viscount Kilmorey1
M, #247383, d. January 1657
Robert Needham, 3rd Viscount Kilmorey was the son of Robert Needham, 2nd Viscount Kilmorey and Frances Anderson.1,2 He married Frances Gerard, daughter of Gilbert Gerard, 2nd Baron Gerard of Gerard's Bromley and Eleanor Dutton.1 He died in January 1657.1
He succeeded as the 3rd Viscount Kilmorey, in Queen's Co. [I., 1625] on 12 September 1653.2
Child of Robert Needham, 3rd Viscount Kilmorey and Frances Gerard
Hon. Frances Needham+3
[S6] G.E. Cokayne; with Vicary Gibbs, H.A. Doubleday, Geoffrey H. White, Duncan Warrand and Lord Howard de Walden, editors, The Complete Peerage of England, Scotland, Ireland, Great Britain and the United Kingdom, Extant, Extinct or Dormant, new ed., 13 volumes in 14 (1910-1959; reprint in 6 volumes, Gloucester, U.K.: Alan Sutton Publishing, 2000), volume VII, page 261. Hereinafter cited as The Complete Peerage.
Frances Gerard1
F, #247384, d. circa May 1636
Last Edited=13 Mar 2009
Frances Gerard was the daughter of Gilbert Gerard, 2nd Baron Gerard of Gerard's Bromley and Eleanor Dutton.1 She married Robert Needham, 3rd Viscount Kilmorey, son of Robert Needham, 2nd Viscount Kilmorey and Frances Anderson.1 She died circa May 1636.1 She was buried on 25 May 1636.2
Her married name became Needham.1
Child of Frances Gerard and Robert Needham, 3rd Viscount Kilmorey
Elizabeth Calveley1
Elizabeth Calveley is the daughter of Sir George Calveley.1 She married Thomas Cotton, son of George Cotton and Mary Bromley.1
Her married name became Cotton.1
Child of Elizabeth Calveley and Thomas Cotton
Sir Robert Cotton, 1st Bt.+2 b. c 1635, d. 17 Dec 1712
Sir George Calveley1
Sir George Calveley lived at Lea, Cheshire, EnglandG.1
Child of Sir George Calveley
Elizabeth Calveley+1
Mary Clare Madden1
Mary Clare Madden is the daughter of William E. Madden.1 She married Sir John Ernest Michael Conant, 2nd Bt., son of Sir Roger John Edward Conant, 1st Bt. and Daphne Lorraine Learoyd, on 11 July 1992.1
From 11 July 1992, her married name became Conant.1
Sir John Salusbury, 4th Bt.1
M, #247388, b. after 1637, d. 23 May 1684
Sir John Salusbury, 4th Bt. was born after 1637.2 He was the son of Sir Thomas Salusbury, 2nd Bt. and Hester Tyrrell.1,3 He married Jane Williams, daughter of Edward Williams, on 29 April 1664 at Llanrwst, Denbighshire, Wales.4,5 He died on 23 May 1684, without issue.4
He lived at Llewenny, Denbighshire, WalesG.1 He gained the title of 4th Baronet Salusbury.
[S15] George Edward Cokayne, editor, The Complete Baronetage, 5 volumes (no date (c. 1900); reprint, Gloucester, U.K.: Alan Sutton Publishing, 1983), volume I, page 128. Hereinafter cited as The Complete Baronetage.
[S229] Burke John and John Bernard Burke, A Genealogical and Heraldic History of the Extinct and Dormant Baronetcies of England (1841, reprint; Baltimore, Maryland, USA: Genealogical Publishing Company, 1985), page 405. Hereinafter cited as Extinct and Dormant Baronetcies of England.
[S4567] Bill Norton, "re: Pitman Family," e-mail message to Darryl Roger LUNDY (101053), 6 April 2010 and 19 April 2011. Hereinafter cited as "re: Pitman Family."
Sir Thomas Lynch1
Last Edited=30 Sep 2011
Sir Thomas Lynch married Mary Temple, daughter of Thomas Temple.2
He lived at Esher, Surrey, EnglandG.1 He held the office of Governor of Jamaica.1
Child of Sir Thomas Lynch
Philadephia Lynch+1 d. 30 Dec 1758
Thomas King1
Thomas King married Philadephia Lynch, daughter of Sir Thomas Lynch.1


text:
About Taranaki
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Taranaki 2050
Songs of Love, War & Peace
Visit > Whats On > Songs of Love, War & Peace
Back To Whats On
Ars Nova Choir's 2019 Concert Season continues with "Songs of Love, War & Peace". Composers throughout the centuries have been fascinated with writing music expressing the hope for peace, the victory at war and the passion for a loved one. This concert features songs of the Victorian age through to the 20th century highlighting these many facets of life accompanied by new orchestrations for a small ensemble of wind and string instruments. Included among the works performed will be movements from Sir Karl Jenkins' well-known choral work "The Armed Man". "Songs of Love, War & Peace" by Ars Nova Choir and accompanied by Ars Antiqua Chamber Ensemble will take place on Saturday 17 August at 2.00pm at St Andrew's Presbyterian Church on Liardet Street, New Plymouth. Admission is $20 and Students $5 - ticket sales at the door. We look forward to seeing you!
Contact Details & Additional Info
70 Liardet St, New Plymouth, Taranaki
Sat 17 Aug, 2:00 p.m.
St Andrew's Presbyterian Church, New Plymouth, Taranaki
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