Tag Archives: science-

Johns Hopkins University | Coursera

Posted: December 2, 2016 at 12:31 pm

Statistics for Genomic Data Science

Starts Dec 19, 2016

Introduction to Systematic Review and Meta-Analysis

Starts Nov 28, 2016

Principles of fMRI 2

Starts Nov 28, 2016

Systems Thinking In Public Health

Starts Dec 12, 2016

Advanced Linear Models for Data Science 1: Least Squares

Starts Nov 28, 2016

Introduction to Neurohacking In R

Starts Dec 12, 2016

Building Data Visualization Tools

Starting December 12th, 2016

Design and Interpretation of Clinical Trials

Starts Dec 05, 2016

Ruby on Rails Web Services and Integration with MongoDB

Starts Dec 05, 2016

Rails with Active Record and Action Pack

Starts Dec 05, 2016

Major Depression in the Population: A Public Health Approach

Starts Dec 05, 2016

Introduction to Genomic Technologies

Starts Dec 19, 2016

Genomic Data Science Capstone

Starts Dec 05, 2016

R Programming Capstone

Starting January 18th, 2016

Training and Learning Programs for Volunteer Community Health Workers

Starts Jan 16, 2017

Mathematical Biostatistics Boot Camp 2

Starts Dec 19, 2016

Reproducible Research

Starts Nov 28, 2016

Statistical Inference

Starts Nov 28, 2016

The Data Scientists Toolbox

Starts Nov 28, 2016

Single Page Web Applications with AngularJS

Starts Dec 05, 2016

Exploratory Data Analysis

Starts Nov 28, 2016

Health for All Through Primary Health Care

Starts Dec 25, 2016

Developing Data Products

Starts Nov 28, 2016

Getting and Cleaning Data

Starts Nov 28, 2016

Ruby on Rails: An Introduction

Starts Dec 05, 2016

Introduction to the Biology of Cancer

Starts Dec 05, 2016

Data Science in Real Life

Starts Nov 28, 2016

Statistical Reasoning for Public Health 2: Regression Methods

Starts Nov 28, 2016

HTML, CSS, and Javascript for Web Developers

Starts Dec 05, 2016

Statistical Reasoning for Public Health 1: Estimation, Inference, & Interpretation

Starts Jan 16, 2017

Understanding Cancer Metastasis

Starts Dec 12, 2016

Systems Science and Obesity

Starts Nov 28, 2016

Data Science Capstone

Starts Feb 06, 2017

Command Line Tools for Genomic Data Science

Starts Dec 19, 2016

The R Programming Environment

Starts Nov 28, 2016

Psychological First Aid

Starts Dec 12, 2016

Mathematical Biostatistics Boot Camp 1

Starts Dec 19, 2016

R Programming

Starts Nov 28, 2016

Building R Packages

Starts Nov 28, 2016

Capstone: Photo Tourist Web Application

Starting January 17, 2017

Confronting Gender Based Violence: Global Lessons for Healthcare Workers

Starts Jan 09, 2017

Community Change in Public Health

Starts Nov 28, 2016

Managing Data Analysis

Starts Nov 28, 2016

Principles of fMRI 1

Starts Dec 19, 2016

Advanced R Programming

Starts Nov 28, 2016

Chemicals and Health

Starts Dec 26, 2016

Python for Genomic Data Science

Starts Dec 19, 2016

Advanced Linear Models for Data Science 2: Statistical Linear Models

Starts Dec 05, 2016

Algorithms for DNA Sequencing

Starts Dec 19, 2016

Practical Machine Learning

Starts Nov 28, 2016

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Johns Hopkins University | Coursera

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Social Origins of Eugenics

Posted: at 12:30 pm

Scientific Origins of Eugenics

Elof Carlson, State University of New York at Stony Brook

The eugenics movement arose in the 20th century as two wings of a common philosophy of human worth. Francis Galton, who coined the term eugenics in 1883, perceived it as a moral philosophy to improve humanity by encouraging the ablest and healthiest people to have more children. The Galtonian ideal of eugenics is usually termed positive eugenics. Negative eugenics, on the other hand, advocated culling the least able from the breeding population to preserve humanity’s fitness. The eugenics movements in the United States, Germany, and Scandinavia favored the negative approach.

The notion of segregating people considered unfit to reproduce dates back to antiquity. For example, the Old Testament describes the Amalekites a supposedly depraved group that God condemned to death. Concerns about environmental influences that might damage heredity leading to ill health, early death, insanity, and defective offspring were formalized in the early 1700s as degeneracy theory. Degeneracy theory maintained a strong scientific following until late in the 19th century. Masturbation, then called onanism, was presented in medical schools as the first biological theory of the cause of degeneracy. Fear of degeneracy through masturbation led Harry Clay Sharp, a prison physician in Jeffersonville, Indiana, to carry out vasectomies on prisoners beginning in 1899. The advocacy of Sharp and his medical colleagues, culminated in an Indiana law mandating compulsory sterilization of “degenerates.” Enacted in 1907, this was the first eugenic sterilization law in the United States.

By the mid-19th century most scientists believed bad environments caused degenerate heredity. Benedict Morel’s work extended the causes of degeneracy to some legitimate agents including poisoning by mercury, ergot, and other toxic substances in the environment. The sociologist Richard Dugdale believed that good environments could transform degenerates into worthy citizens within three generations. This position was a backdrop to his very influential study on The Jukes (1877), a degenerate family of paupers and petty criminals in Ulster County, New York. The inheritance of acquired (environmental) characters was challenged in the 1880s by August Weismann, whose theory of the germ plasm convinced most scientists that changes in body tissue (the soma) had little or no effect on reproductive tissue (the germ plasm). At the beginning of the 20th century, Weismann’s views were absorbed by degeneracy theorists who embraced negative eugenics as their favored model.

Adherents of the new field of genetics were ambivalent about eugenics. Most basic scientists including William Bateson in Great Britain, and Thomas Hunt Morgan in the United States shunned eugenics as vulgar and an unproductive field for research. However, Bateson’s and Morgan’s contributions to basic genetics were quickly absorbed by eugenicists, who took interest in Mendelian analysis of pedigrees of humans, plants, and animals. Many eugenicists had some type of agricultural background. Charles Davenport and Harry Laughlin, who together ran the Eugenics Record Office, were introduced through their shared interest in chicken breeding. Both also were active in Eugenics Section of the American Breeder’s Association (ABA). Davenport’s book, Eugenics: The Science of Human Improvement through Better Breeding, had a distinct agricultural flavor, and his affiliation with the ABA was included under his name on the title page. Agricultural genetics also provided the favored model for negative eugenics: human populations, like agricultural breeds and varieties, had to be culled of their least productive members, with only the healthiest specimens used for breeding.

Evolutionary models of natural selection and dysgenic (bad) hereditary practices in society also contributed to eugenic theory. For example, there was fear that highly intelligent people would have smaller families (about 2 children), while the allegedly degenerate elements of society were having larger families of four to eight children. Public welfare might also play a role in allowing less fit people to survive and reproduce, further upsetting the natural selection of fitter people.

Medicine also put its stamp on eugenics. Physicians like Anton Ochsner and Harry Sharp were convinced that social failure was a medical problem. Italian criminologist and physician Cesare Lombroso popularized the image of an innate criminal type that was thought to be a reversion or atavism of a bestial ancestor of humanity. When medical means failed to help the psychotic, the retarded, the pauper, and the vagrant, eugenicists shifted to preventive medicine. The German physician-legislator Rudolph Virchow, advocated programs to deal with disease prevention on a large scale. Virchow’s public health movement was fused with eugenics to form the racial hygiene movement in Germany and came to America through physicians he trained.

Eugenicists argued that “defectives” should be prevented from breeding, through custody in asylums or compulsory sterilization. Most doctors probably felt that sterilization was a more humane way of dealing with people who could not help themselves. Vasectomy and tubal ligation were favored methods, because they did not alter the physiological and psychological contribution of the reproductive organs. Sterilization allowed the convicted criminal or mental patient to participate in society, rather than being institutionalized at public expense. Sterilization was not viewed as a punishment because these doctors believed (erroneously) that the social failure of “unfit” people was due to an irreversibly degenerate germ plasm.

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Social Origins of Eugenics

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UK teenager wins battle to have body cryogenically frozen – CNN

Posted: November 25, 2016 at 10:13 am

The girl — who can’t be identified and is referred to only as “JS” — suffered from a rare form of cancer and expressed a hope to be brought back to life and cured in the future.

She died on October 17 but details of the case at London’s High Court were not allowed to be made public until now.

In his judgment, obtained by CNN, Mr. Justice Peter Jackson said the girl had expressed her desire to be cryogenically frozen.

She wrote: “I have been asked to explain why I want this unusual thing done. I’m only 14 years old and I don’t want to die, but I know I am going to. I think being cryo-preserved gives me a chance to be cured and woken up, even in hundreds of years’ time. I don’t want to be buried underground.

“I want to live and live longer and I think that in the future they might find a cure for my cancer and wake me up. I want to have this chance. This is my wish.”

According to the judgment, the girl’s parents are divorced and their relationship is “very bad.” Her mother was supportive of her wish, but her father — who had not seen his daughter face-to-face since 2008 — initially was not.

At the start of proceedings, the teenager’s father, who also has cancer, wrote: “Even if the treatment is successful and [JS] is brought back to life in let’s say 200 years, she may not find any relative and she might not remember things and she may be left in a desperate situation given that she is only 14 years old and will be in the United States of America.”

However, he subsequently changed his position, saying he “respected the decisions” his daughter was making.

The judge said this fluctuation in his views was understandable, adding, “No other parent has ever been put in his position.”

But he emphasized he was not ruling on the science of cryonics, but rather on the dispute between her parents over who was responsible for the arrangements after her death.

The judge also said there was no doubt the girl — described as “a bright, intelligent young person who is able to articulate strongly held views on her current situation” — had the capacity to start legal action.

“Over recent months, JS has used the internet to investigate cryonics: the freezing of a dead body in the hope that resuscitation and a cure may be possible in the distant future,” he said.

“The scientific theory underlying cryonics is speculative and controversial, and there is considerable debate about its ethical implications.

“On the other hand, cryopreservation, the preservation of cells and tissues by freezing, is now a well-known process in certain branches of medicine, for example the preservation of sperm and embryos as part of fertility treatment.

“Cryonics is cryopreservation taken to its extreme.”

The judge ruled in favor of her mother and said the girl had died peacefully, knowing her wishes had been met.

But he cautioned that hospital officials had had “real misgivings” about the way the process was handled on the day she died.

The girl’s mother was said to have been preoccupied with the arrangements after her death, rather than being fully available to her child, he said, and the voluntary organization which helped get her body ready for preservation was disorganized.

The case was said by the judge to be the only one of its kind to have come before the courts in England and Wales, and probably anywhere else. “It is an example of the new questions that science poses to the law, perhaps most of all to family law,” he added.

The cost of the procedure in the United States — which the judge said was about 37,000 ($46,000) — is being met by her maternal grandparents, he said, although the family is not well off. They chose the most basic arrangement, he said, which “simply involves the freezing of the body in perpetuity.”

The Cryonics Institute, which is based in Michigan, said the body of a 14-year-old girl from London arrived at its facility, packed in dry ice, on October 25, about eight days after her death.

“The patient was then placed in the computer controlled cooling chamber to cool to liquid nitrogen temperature,” a statement posted on its website said.

“The human cooling program from dry ice was selected and the time needed to cool the patient to liquid nitrogen temperature was 24 hours. The patient was then placed in a cryostat for longterm cryonic storage.”

The Cryonics Institute said the girl was its 143rd patient.

Its website explains the process as “a technique intended to hopefully save lives and greatly extend lifespan. It involves cooling legally-dead people to liquid nitrogen temperature where physical decay essentially stops, in the hope that future scientific procedures will someday revive them and restore them to youth and good health.

“A person held in such a state is said to be a ‘cryopreserved patient’, because we do not regard the cryopreserved person as being inevitably ‘dead’.”

However, some skepticism remains about the science of cryogenics.

Barry Fuller, professor in Surgical Science and Low Temperature Medicine at University College London, said that cryopreservation “has many useful applications in day to day medicine, such as cryopreserving blood cells, sperm and embryos.”

But, he said, “cryopreservation has not yet been successfully applied to large structures, such as human kidneys for transplantation, because we have not yet adequately been able to produce suitable equipment to optimize all the steps.

“This is why we have to say that at the moment we have no objective evidence that a whole human body can survive cryopreservation with cells which will function after rearming.”

CNN’s Simon Cullen and Meera Senthilingam contributed to this report.

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UK teenager wins battle to have body cryogenically frozen – CNN

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What does artificial intelligence mean? – Definitions.net

Posted: November 23, 2016 at 10:00 pm

Artificial intelligence

Artificial intelligence is technology and a branch of computer science that studies and develops intelligent machines and software. Major AI researchers and textbooks define the field as “the study and design of intelligent agents”, where an intelligent agent is a system that perceives its environment and takes actions that maximize its chances of success. John McCarthy, who coined the term in 1955, defines it as “the science and engineering of making intelligent machines”. AI research is highly technical and specialised, deeply divided into subfields that often fail to communicate with each other. Some of the division is due to social and cultural factors: subfields have grown up around particular institutions and the work of individual researchers. AI research is also divided by several technical issues. There are subfields which are focused on the solution of specific problems, on one of several possible approaches, on the use of widely differing tools and towards the accomplishment of particular applications. The central problems of AI research include reasoning, knowledge, planning, learning, communication, perception and the ability to move and manipulate objects. General intelligence is still among the field’s long term goals. Currently popular approaches include statistical methods, computational intelligence and traditional symbolic AI. There are an enormous number of tools used in AI, including versions of search and mathematical optimization, logic, methods based on probability and economics, and many others.

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What does artificial intelligence mean? – Definitions.net

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Gene – Wikipedia

Posted: at 9:56 pm

This article is about the heritable unit for transmission of biological traits. For other uses, see Gene (disambiguation).

A gene is a locus (or region) of DNA which is made up of nucleotides and is the molecular unit of heredity.[1][2]:Glossary The transmission of genes to an organism’s offspring is the basis of the inheritance of phenotypic traits. Most biological traits are under the influence of polygenes (many different genes) as well as geneenvironment interactions. Some genetic traits are instantly visible, such as eye colour or number of limbs, and some are not, such as blood type, risk for specific diseases, or the thousands of basic biochemical processes that comprise life.

Genes can acquire mutations in their sequence, leading to different variants, known as alleles, in the population. These alleles encode slightly different versions of a protein, which cause different phenotype traits. Colloquial usage of the term “having a gene” (e.g., “good genes,” “hair colour gene”) typically refers to having a different allele of the gene. Genes evolve due to natural selection or survival of the fittest of the alleles.

The concept of a gene continues to be refined as new phenomena are discovered.[3] For example, regulatory regions of a gene can be far removed from its coding regions, and coding regions can be split into several exons. Some viruses store their genome in RNA instead of DNA and some gene products are functional non-coding RNAs. Therefore, a broad, modern working definition of a gene is any discrete locus of heritable, genomic sequence which affect an organism’s traits by being expressed as a functional product or by regulation of gene expression.[4][5]

The existence of discrete inheritable units was first suggested by Gregor Mendel (18221884).[6] From 1857 to 1864, he studied inheritance patterns in 8000 common edible pea plants, tracking distinct traits from parent to offspring. He described these mathematically as 2ncombinations where n is the number of differing characteristics in the original peas. Although he did not use the term gene, he explained his results in terms of discrete inherited units that give rise to observable physical characteristics. This description prefigured the distinction between genotype (the genetic material of an organism) and phenotype (the visible traits of that organism). Mendel was also the first to demonstrate independent assortment, the distinction between dominant and recessive traits, the distinction between a heterozygote and homozygote, and the phenomenon of discontinuous inheritance.

Prior to Mendel’s work, the dominant theory of heredity was one of blending inheritance, which suggested that each parent contributed fluids to the fertilisation process and that the traits of the parents blended and mixed to produce the offspring. Charles Darwin developed a theory of inheritance he termed pangenesis, from Greek pan (“all, whole”) and genesis (“birth”) / genos (“origin”).[7][8] Darwin used the term gemmule to describe hypothetical particles that would mix during reproduction.

Mendel’s work went largely unnoticed after its first publication in 1866, but was rediscovered in the late 19th century by Hugo de Vries, Carl Correns, and Erich von Tschermak, who (claimed to have) reached similar conclusions in their own research.[9] Specifically, in 1889, Hugo de Vries published his book Intracellular Pangenesis,[10] in which he postulated that different characters have individual hereditary carriers and that inheritance of specific traits in organisms comes in particles. De Vries called these units “pangenes” (Pangens in German), after Darwin’s 1868 pangenesis theory.

Sixteen years later, in 1905, the word genetics was first used by William Bateson,[11] while Eduard Strasburger, amongst others, still used the term pangene for the fundamental physical and functional unit of heredity.[12] In 1909 the Danish botanist Wilhelm Johannsen shortened the name to “gene”. [13]

Advances in understanding genes and inheritance continued throughout the 20th century. Deoxyribonucleic acid (DNA) was shown to be the molecular repository of genetic information by experiments in the 1940s to 1950s.[14][15] The structure of DNA was studied by Rosalind Franklin and Maurice Wilkins using X-ray crystallography, which led James D. Watson and Francis Crick to publish a model of the double-stranded DNA molecule whose paired nucleotide bases indicated a compelling hypothesis for the mechanism of genetic replication.[16][17]

In the early 1950s the prevailing view was that the genes in a chromosome acted like discrete entities, indivisible by recombination and arranged like beads on a string. The experiments of Benzer using mutants defective in the rII region of bacteriophage T4 (1955-1959) showed that individual genes have a simple linear structure and are likely to be equivalent to a linear section of DNA.[18][19]

Collectively, this body of research established the central dogma of molecular biology, which states that proteins are translated from RNA, which is transcribed from DNA. This dogma has since been shown to have exceptions, such as reverse transcription in retroviruses. The modern study of genetics at the level of DNA is known as molecular genetics.

In 1972, Walter Fiers and his team at the University of Ghent were the first to determine the sequence of a gene: the gene for Bacteriophage MS2 coat protein.[20] The subsequent development of chain-termination DNA sequencing in 1977 by Frederick Sanger improved the efficiency of sequencing and turned it into a routine laboratory tool.[21] An automated version of the Sanger method was used in early phases of the Human Genome Project.[22]

The theories developed in the 1930s and 1940s to integrate molecular genetics with Darwinian evolution are called the modern evolutionary synthesis, a term introduced by Julian Huxley.[23] Evolutionary biologists subsequently refined this concept, such as George C. Williams’ gene-centric view of evolution. He proposed an evolutionary concept of the gene as a unit of natural selection with the definition: “that which segregates and recombines with appreciable frequency.”[24]:24 In this view, the molecular gene transcribes as a unit, and the evolutionary gene inherits as a unit. Related ideas emphasizing the centrality of genes in evolution were popularized by Richard Dawkins.[25][26]

The vast majority of living organisms encode their genes in long strands of DNA (deoxyribonucleic acid). DNA consists of a chain made from four types of nucleotide subunits, each composed of: a five-carbon sugar (2′-deoxyribose), a phosphate group, and one of the four bases adenine, cytosine, guanine, and thymine.[2]:2.1

Two chains of DNA twist around each other to form a DNA double helix with the phosphate-sugar backbone spiralling around the outside, and the bases pointing inwards with adenine base pairing to thymine and guanine to cytosine. The specificity of base pairing occurs because adenine and thymine align to form two hydrogen bonds, whereas cytosine and guanine form three hydrogen bonds. The two strands in a double helix must therefore be complementary, with their sequence of bases matching such that the adenines of one strand are paired with the thymines of the other strand, and so on.[2]:4.1

Due to the chemical composition of the pentose residues of the bases, DNA strands have directionality. One end of a DNA polymer contains an exposed hydroxyl group on the deoxyribose; this is known as the 3’end of the molecule. The other end contains an exposed phosphate group; this is the 5’end. The two strands of a double-helix run in opposite directions. Nucleic acid synthesis, including DNA replication and transcription occurs in the 5’3’direction, because new nucleotides are added via a dehydration reaction that uses the exposed 3’hydroxyl as a nucleophile.[27]:27.2

The expression of genes encoded in DNA begins by transcribing the gene into RNA, a second type of nucleic acid that is very similar to DNA, but whose monomers contain the sugar ribose rather than deoxyribose. RNA also contains the base uracil in place of thymine. RNA molecules are less stable than DNA and are typically single-stranded. Genes that encode proteins are composed of a series of three-nucleotide sequences called codons, which serve as the “words” in the genetic “language”. The genetic code specifies the correspondence during protein translation between codons and amino acids. The genetic code is nearly the same for all known organisms.[2]:4.1

The total complement of genes in an organism or cell is known as its genome, which may be stored on one or more chromosomes. A chromosome consists of a single, very long DNA helix on which thousands of genes are encoded.[2]:4.2 The region of the chromosome at which a particular gene is located is called its locus. Each locus contains one allele of a gene; however, members of a population may have different alleles at the locus, each with a slightly different gene sequence.

The majority of eukaryotic genes are stored on a set of large, linear chromosomes. The chromosomes are packed within the nucleus in complex with storage proteins called histones to form a unit called a nucleosome. DNA packaged and condensed in this way is called chromatin.[2]:4.2 The manner in which DNA is stored on the histones, as well as chemical modifications of the histone itself, regulate whether a particular region of DNA is accessible for gene expression. In addition to genes, eukaryotic chromosomes contain sequences involved in ensuring that the DNA is copied without degradation of end regions and sorted into daughter cells during cell division: replication origins, telomeres and the centromere.[2]:4.2 Replication origins are the sequence regions where DNA replication is initiated to make two copies of the chromosome. Telomeres are long stretches of repetitive sequence that cap the ends of the linear chromosomes and prevent degradation of coding and regulatory regions during DNA replication. The length of the telomeres decreases each time the genome is replicated and has been implicated in the aging process.[29] The centromere is required for binding spindle fibres to separate sister chromatids into daughter cells during cell division.[2]:18.2

Prokaryotes (bacteria and archaea) typically store their genomes on a single large, circular chromosome. Similarly, some eukaryotic organelles contain a remnant circular chromosome with a small number of genes.[2]:14.4 Prokaryotes sometimes supplement their chromosome with additional small circles of DNA called plasmids, which usually encode only a few genes and are transferable between individuals. For example, the genes for antibiotic resistance are usually encoded on bacterial plasmids and can be passed between individual cells, even those of different species, via horizontal gene transfer.[30]

Whereas the chromosomes of prokaryotes are relatively gene-dense, those of eukaryotes often contain regions of DNA that serve no obvious function. Simple single-celled eukaryotes have relatively small amounts of such DNA, whereas the genomes of complex multicellular organisms, including humans, contain an absolute majority of DNA without an identified function.[31] This DNA has often been referred to as “junk DNA”. However, more recent analyses suggest that, although protein-coding DNA makes up barely 2% of the human genome, about 80% of the bases in the genome may be expressed, so the term “junk DNA” may be a misnomer.[5]

The structure of a gene consists of many elements of which the actual protein coding sequence is often only a small part. These include DNA regions that are not transcribed as well as untranslated regions of the RNA.

Firstly, flanking the open reading frame, all genes contain a regulatory sequence that is required for their expression. In order to be expressed, genes require a promoter sequence. The promoter is recognized and bound by transcription factors and RNA polymerase to initiate transcription.[2]:7.1 A gene can have more than one promoter, resulting in messenger RNAs (mRNA) that differ in how far they extend in the 5’end.[32] Promoter regions have a consensus sequence, however highly transcribed genes have “strong” promoter sequences that bind the transcription machinery well, whereas others have “weak” promoters that bind poorly and initiate transcription less frequently.[2]:7.2Eukaryotic promoter regions are much more complex and difficult to identify than prokaryotic promoters.[2]:7.3

Additionally, genes can have regulatory regions many kilobases upstream or downstream of the open reading frame. These act by binding to transcription factors which then cause the DNA to loop so that the regulatory sequence (and bound transcription factor) become close to the RNA polymerase binding site.[33] For example, enhancers increase transcription by binding an activator protein which then helps to recruit the RNA polymerase to the promoter; conversely silencers bind repressor proteins and make the DNA less available for RNA polymerase.[34]

The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.[35] In addition, most eukaryotic open reading frames contain untranslated introns which are removed before the exons are translated. The sequences at the ends of the introns, dictate the splice sites to generate the final mature mRNA which encodes the protein or RNA product.[36]

Many prokaryotic genes are organized into operons, with multiple protein-coding sequences that are transcribed as a unit.[37][38] The genes in an operon are transcribed as a continuous messenger RNA, referred to as a polycistronic mRNA. The term cistron in this context is equivalent to gene. The transcription of an operons mRNA is often controlled by a repressor that can occur in an active or inactive state depending on the presence of certain specific metabolites.[39] When active, the repressor binds to a DNA sequence at the beginning of the operon, called the operator region, and represses transcription of the operon; when the repressor is inactive transcription of the operon can occur (see e.g. Lac operon). The products of operon genes typically have related functions and are involved in the same regulatory network.[2]:7.3

Defining exactly what section of a DNA sequence comprises a gene is difficult.[3]Regulatory regions of a gene such as enhancers do not necessarily have to be close to the coding sequence on the linear molecule because the intervening DNA can be looped out to bring the gene and its regulatory region into proximity. Similarly, a gene’s introns can be much larger than its exons. Regulatory regions can even be on entirely different chromosomes and operate in trans to allow regulatory regions on one chromosome to come in contact with target genes on another chromosome.[40][41]

Early work in molecular genetics suggested the concept that one gene makes one protein. This concept (originally called the one gene-one enzyme hypothesis) emerged from an influential 1941 paper by George Beadle and Edward Tatum on experiments with mutants of the fungus Neurospora crassa.[42]Norman Horowitz, an early colleague on the Neurospora research, reminisced in 2004 that these experiments founded the science of what Beadle and Tatum called biochemical genetics. In actuality they proved to be the opening gun in what became molecular genetics and all the developments that have followed from that.[43] The one gene-one protein concept has been refined since the discovery of genes that can encode multiple proteins by alternative splicing and coding sequences split in short section across the genome whose mRNAs are concatenated by trans-splicing.[5][44][45]

A broad operational definition is sometimes used to encompass the complexity of these diverse phenomena, where a gene is defined as a union of genomic sequences encoding a coherent set of potentially overlapping functional products.[11] This definition categorizes genes by their functional products (proteins or RNA) rather than their specific DNA loci, with regulatory elements classified as gene-associated regions.[11]

In all organisms, two steps are required to read the information encoded in a gene’s DNA and produce the protein it specifies. First, the gene’s DNA is transcribed to messenger RNA (mRNA).[2]:6.1 Second, that mRNA is translated to protein.[2]:6.2 RNA-coding genes must still go through the first step, but are not translated into protein.[46] The process of producing a biologically functional molecule of either RNA or protein is called gene expression, and the resulting molecule is called a gene product.

The nucleotide sequence of a gene’s DNA specifies the amino acid sequence of a protein through the genetic code. Sets of three nucleotides, known as codons, each correspond to a specific amino acid.[2]:6 The principle that three sequential bases of DNA code for each amino acid was demonstrated in 1961 using frameshift mutations in the rIIB gene of bacteriophage T4[47] (see Crick, Brenner et al. experiment).

Additionally, a “start codon”, and three “stop codons” indicate the beginning and end of the protein coding region. There are 64possible codons (four possible nucleotides at each of three positions, hence 43possible codons) and only 20standard amino acids; hence the code is redundant and multiple codons can specify the same amino acid. The correspondence between codons and amino acids is nearly universal among all known living organisms.[48]

Transcription produces a single-stranded RNA molecule known as messenger RNA, whose nucleotide sequence is complementary to the DNA from which it was transcribed.[2]:6.1 The mRNA acts as an intermediate between the DNA gene and its final protein product. The gene’s DNA is used as a template to generate a complementary mRNA. The mRNA matches the sequence of the gene’s DNA coding strand because it is synthesised as the complement of the template strand. Transcription is performed by an enzyme called an RNA polymerase, which reads the template strand in the 3′ to 5’direction and synthesizes the RNA from 5′ to 3′. To initiate transcription, the polymerase first recognizes and binds a promoter region of the gene. Thus, a major mechanism of gene regulation is the blocking or sequestering the promoter region, either by tight binding by repressor molecules that physically block the polymerase, or by organizing the DNA so that the promoter region is not accessible.[2]:7

In prokaryotes, transcription occurs in the cytoplasm; for very long transcripts, translation may begin at the 5’end of the RNA while the 3’end is still being transcribed. In eukaryotes, transcription occurs in the nucleus, where the cell’s DNA is stored. The RNA molecule produced by the polymerase is known as the primary transcript and undergoes post-transcriptional modifications before being exported to the cytoplasm for translation. One of the modifications performed is the splicing of introns which are sequences in the transcribed region that do not encode protein. Alternative splicing mechanisms can result in mature transcripts from the same gene having different sequences and thus coding for different proteins. This is a major form of regulation in eukaryotic cells and also occurs in some prokaryotes.[2]:7.5[49]

Translation is the process by which a mature mRNA molecule is used as a template for synthesizing a new protein.[2]:6.2 Translation is carried out by ribosomes, large complexes of RNA and protein responsible for carrying out the chemical reactions to add new amino acids to a growing polypeptide chain by the formation of peptide bonds. The genetic code is read three nucleotides at a time, in units called codons, via interactions with specialized RNA molecules called transfer RNA (tRNA). Each tRNA has three unpaired bases known as the anticodon that are complementary to the codon it reads on the mRNA. The tRNA is also covalently attached to the amino acid specified by the complementary codon. When the tRNA binds to its complementary codon in an mRNA strand, the ribosome attaches its amino acid cargo to the new polypeptide chain, which is synthesized from amino terminus to carboxyl terminus. During and after synthesis, most new proteins must fold to their active three-dimensional structure before they can carry out their cellular functions.[2]:3

Genes are regulated so that they are expressed only when the product is needed, since expression draws on limited resources.[2]:7 A cell regulates its gene expression depending on its external environment (e.g. available nutrients, temperature and other stresses), its internal environment (e.g. cell division cycle, metabolism, infection status), and its specific role if in a multicellular organism. Gene expression can be regulated at any step: from transcriptional initiation, to RNA processing, to post-translational modification of the protein. The regulation of lactose metabolism genes in E. coli (lac operon) was the first such mechanism to be described in 1961.[50]

A typical protein-coding gene is first copied into RNA as an intermediate in the manufacture of the final protein product.[2]:6.1 In other cases, the RNA molecules are the actual functional products, as in the synthesis of ribosomal RNA and transfer RNA. Some RNAs known as ribozymes are capable of enzymatic function, and microRNA has a regulatory role. The DNA sequences from which such RNAs are transcribed are known as non-coding RNA genes.[46]

Some viruses store their entire genomes in the form of RNA, and contain no DNA at all.[51][52] Because they use RNA to store genes, their cellular hosts may synthesize their proteins as soon as they are infected and without the delay in waiting for transcription.[53] On the other hand, RNA retroviruses, such as HIV, require the reverse transcription of their genome from RNA into DNA before their proteins can be synthesized. RNA-mediated epigenetic inheritance has also been observed in plants and very rarely in animals.[54]

Organisms inherit their genes from their parents. Asexual organisms simply inherit a complete copy of their parent’s genome. Sexual organisms have two copies of each chromosome because they inherit one complete set from each parent.[2]:1

According to Mendelian inheritance, variations in an organism’s phenotype (observable physical and behavioral characteristics) are due in part to variations in its genotype (particular set of genes). Each gene specifies a particular trait with different sequence of a gene (alleles) giving rise to different phenotypes. Most eukaryotic organisms (such as the pea plants Mendel worked on) have two alleles for each trait, one inherited from each parent.[2]:20

Alleles at a locus may be dominant or recessive; dominant alleles give rise to their corresponding phenotypes when paired with any other allele for the same trait, whereas recessive alleles give rise to their corresponding phenotype only when paired with another copy of the same allele. For example, if the allele specifying tall stems in pea plants is dominant over the allele specifying short stems, then pea plants that inherit one tall allele from one parent and one short allele from the other parent will also have tall stems. Mendel’s work demonstrated that alleles assort independently in the production of gametes, or germ cells, ensuring variation in the next generation. Although Mendelian inheritance remains a good model for many traits determined by single genes (including a number of well-known genetic disorders) it does not include the physical processes of DNA replication and cell division.[55][56]

The growth, development, and reproduction of organisms relies on cell division, or the process by which a single cell divides into two usually identical daughter cells. This requires first making a duplicate copy of every gene in the genome in a process called DNA replication.[2]:5.2 The copies are made by specialized enzymes known as DNA polymerases, which “read” one strand of the double-helical DNA, known as the template strand, and synthesize a new complementary strand. Because the DNA double helix is held together by base pairing, the sequence of one strand completely specifies the sequence of its complement; hence only one strand needs to be read by the enzyme to produce a faithful copy. The process of DNA replication is semiconservative; that is, the copy of the genome inherited by each daughter cell contains one original and one newly synthesized strand of DNA.[2]:5.2

The rate of DNA replication in living cells was first measured as the rate of phage T4 DNA elongation in phage-infected E. coli and found to be impressively rapid.[57] During the period of exponential DNA increase at 37 C, the rate of elongation was 749 nucleotides per second.

After DNA replication is complete, the cell must physically separate the two copies of the genome and divide into two distinct membrane-bound cells.[2]:18.2 In prokaryotes(bacteria and archaea) this usually occurs via a relatively simple process called binary fission, in which each circular genome attaches to the cell membrane and is separated into the daughter cells as the membrane invaginates to split the cytoplasm into two membrane-bound portions. Binary fission is extremely fast compared to the rates of cell division in eukaryotes. Eukaryotic cell division is a more complex process known as the cell cycle; DNA replication occurs during a phase of this cycle known as S phase, whereas the process of segregating chromosomes and splitting the cytoplasm occurs during M phase.[2]:18.1

The duplication and transmission of genetic material from one generation of cells to the next is the basis for molecular inheritance, and the link between the classical and molecular pictures of genes. Organisms inherit the characteristics of their parents because the cells of the offspring contain copies of the genes in their parents’ cells. In asexually reproducing organisms, the offspring will be a genetic copy or clone of the parent organism. In sexually reproducing organisms, a specialized form of cell division called meiosis produces cells called gametes or germ cells that are haploid, or contain only one copy of each gene.[2]:20.2 The gametes produced by females are called eggs or ova, and those produced by males are called sperm. Two gametes fuse to form a diploid fertilized egg, a single cell that has two sets of genes, with one copy of each gene from the mother and one from the father.[2]:20

During the process of meiotic cell division, an event called genetic recombination or crossing-over can sometimes occur, in which a length of DNA on one chromatid is swapped with a length of DNA on the corresponding homologous non-sister chromatid. This can result in reassortment of otherwise linked alleles.[2]:5.5 The Mendelian principle of independent assortment asserts that each of a parent’s two genes for each trait will sort independently into gametes; which allele an organism inherits for one trait is unrelated to which allele it inherits for another trait. This is in fact only true for genes that do not reside on the same chromosome, or are located very far from one another on the same chromosome. The closer two genes lie on the same chromosome, the more closely they will be associated in gametes and the more often they will appear together; genes that are very close are essentially never separated because it is extremely unlikely that a crossover point will occur between them. This is known as genetic linkage.[58]

DNA replication is for the most part extremely accurate, however errors (mutations) do occur.[2]:7.6 The error rate in eukaryotic cells can be as low as 108 per nucleotide per replication,[59][60] whereas for some RNA viruses it can be as high as 103.[61] This means that each generation, each human genome accumulates 12 new mutations.[61] Small mutations can be caused by DNA replication and the aftermath of DNA damage and include point mutations in which a single base is altered and frameshift mutations in which a single base is inserted or deleted. Either of these mutations can change the gene by missense (change a codon to encode a different amino acid) or nonsense (a premature stop codon).[62] Larger mutations can be caused by errors in recombination to cause chromosomal abnormalities including the duplication, deletion, rearrangement or inversion of large sections of a chromosome. Additionally, DNA repair mechanisms can introduce mutational errors when repairing physical damage to the molecule. The repair, even with mutation, is more important to survival than restoring an exact copy, for example when repairing double-strand breaks.[2]:5.4

When multiple different alleles for a gene are present in a species’s population it is called polymorphic. Most different alleles are functionally equivalent, however some alleles can give rise to different phenotypic traits. A gene’s most common allele is called the wild type, and rare alleles are called mutants. The genetic variation in relative frequencies of different alleles in a population is due to both natural selection and genetic drift.[63] The wild-type allele is not necessarily the ancestor of less common alleles, nor is it necessarily fitter.

Most mutations within genes are neutral, having no effect on the organism’s phenotype (silent mutations). Some mutations do not change the amino acid sequence because multiple codons encode the same amino acid (synonymous mutations). Other mutations can be neutral if they lead to amino acid sequence changes, but the protein still functions similarly with the new amino acid (e.g. conservative mutations). Many mutations, however, are deleterious or even lethal, and are removed from populations by natural selection. Genetic disorders are the result of deleterious mutations and can be due to spontaneous mutation in the affected individual, or can be inherited. Finally, a small fraction of mutations are beneficial, improving the organism’s fitness and are extremely important for evolution, since their directional selection leads to adaptive evolution.[2]:7.6

Genes with a most recent common ancestor, and thus a shared evolutionary ancestry, are known as homologs.[64] These genes appear either from gene duplication within an organism’s genome, where they are known as paralogous genes, or are the result of divergence of the genes after a speciation event, where they are known as orthologous genes,[2]:7.6 and often perform the same or similar functions in related organisms. It is often assumed that the functions of orthologous genes are more similar than those of paralogous genes, although the difference is minimal.[65][66]

The relationship between genes can be measured by comparing the sequence alignment of their DNA.[2]:7.6 The degree of sequence similarity between homologous genes is called conserved sequence. Most changes to a gene’s sequence do not affect its function and so genes accumulate mutations over time by neutral molecular evolution. Additionally, any selection on a gene will cause its sequence to diverge at a different rate. Genes under stabilizing selection are constrained and so change more slowly whereas genes under directional selection change sequence more rapidly.[67] The sequence differences between genes can be used for phylogenetic analyses to study how those genes have evolved and how the organisms they come from are related.[68][69]

The most common source of new genes in eukaryotic lineages is gene duplication, which creates copy number variation of an existing gene in the genome.[70][71] The resulting genes (paralogs) may then diverge in sequence and in function. Sets of genes formed in this way comprise a gene family. Gene duplications and losses within a family are common and represent a major source of evolutionary biodiversity.[72] Sometimes, gene duplication may result in a nonfunctional copy of a gene, or a functional copy may be subject to mutations that result in loss of function; such nonfunctional genes are called pseudogenes.[2]:7.6

“Orphan” genes, whose sequence shows no similarity to existing genes, are less common than gene duplicates. Estimates of the number of genes with no homologs outside humans range from 18[73] to 60.[74] Two primary sources of orphan protein-coding genes are gene duplication followed by extremely rapid sequence change, such that the original relationship is undetectable by sequence comparisons, and de novo conversion of a previously non-coding sequence into a protein-coding gene.[75] De novo genes are typically shorter and simpler in structure than most eukaryotic genes, with few if any introns.[70] Over long evolutionary time periods, de novo gene birth may be responsible for a significant fraction of taxonomically-restricted gene families.[76]

Horizontal gene transfer refers to the transfer of genetic material through a mechanism other than reproduction. This mechanism is a common source of new genes in prokaryotes, sometimes thought to contribute more to genetic variation than gene duplication.[77] It is a common means of spreading antibiotic resistance, virulence, and adaptive metabolic functions.[30][78] Although horizontal gene transfer is rare in eukaryotes, likely examples have been identified of protist and alga genomes containing genes of bacterial origin.[79][80]

The genome is the total genetic material of an organism and includes both the genes and non-coding sequences.[81]

The genome size, and the number of genes it encodes varies widely between organisms. The smallest genomes occur in viruses (which can have as few as 2 protein-coding genes),[90] and viroids (which act as a single non-coding RNA gene).[91] Conversely, plants can have extremely large genomes,[92] with rice containing >46,000 protein-coding genes.[93] The total number of protein-coding genes (the Earth’s proteome) is estimated to be 5million sequences.[94]

Although the number of base-pairs of DNA in the human genome has been known since the 1960s, the estimated number of genes has changed over time as definitions of genes, and methods of detecting them have been refined. Initial theoretical predictions of the number of human genes were as high as 2,000,000.[95] Early experimental measures indicated there to be 50,000100,000 transcribed genes (expressed sequence tags).[96] Subsequently, the sequencing in the Human Genome Project indicated that many of these transcripts were alternative variants of the same genes, and the total number of protein-coding genes was revised down to ~20,000[89] with 13 genes encoded on the mitochondrial genome.[87] Of the human genome, only 12% consists of protein-coding genes,[97] with the remainder being ‘noncoding’ DNA such as introns, retrotransposons, and noncoding RNAs.[97][98] Every multicellular organism has all its genes in each cell of its body but not every gene functions in every cell .

Essential genes are the set of genes thought to be critical for an organism’s survival.[100] This definition assumes the abundant availability of all relevant nutrients and the absence of environmental stress. Only a small portion of an organism’s genes are essential. In bacteria, an estimated 250400 genes are essential for Escherichia coli and Bacillus subtilis, which is less than 10% of their genes.[101][102][103] Half of these genes are orthologs in both organisms and are largely involved in protein synthesis.[103] In the budding yeast Saccharomyces cerevisiae the number of essential genes is slightly higher, at 1000 genes (~20% of their genes).[104] Although the number is more difficult to measure in higher eukaryotes, mice and humans are estimated to have around 2000 essential genes (~10% of their genes).[105] The synthetic organism, Syn 3, has a minimal genome of 473 essential genes and quasi-essential genes (necessary for fast growth), although 149 have unknown function.[99]

Essential genes include Housekeeping genes (critical for basic cell functions)[106] as well as genes that are expressed at different times in the organisms development or life cycle.[107] Housekeeping genes are used as experimental controls when analysing gene expression, since they are constitutively expressed at a relatively constant level.

Gene nomenclature has been established by the HUGO Gene Nomenclature Committee (HGNC) for each known human gene in the form of an approved gene name and symbol (short-form abbreviation), which can be accessed through a database maintained by HGNC. Symbols are chosen to be unique, and each gene has only one symbol (although approved symbols sometimes change). Symbols are preferably kept consistent with other members of a gene family and with homologs in other species, particularly the mouse due to its role as a common model organism.[108]

Genetic engineering is the modification of an organism’s genome through biotechnology. Since the 1970s, a variety of techniques have been developed to specifically add, remove and edit genes in an organism.[109] Recently developed genome engineering techniques use engineered nuclease enzymes to create targeted DNA repair in a chromosome to either disrupt or edit a gene when the break is repaired.[110][111][112][113] The related term synthetic biology is sometimes used to refer to extensive genetic engineering of an organism.[114]

Genetic engineering is now a routine research tool with model organisms. For example, genes are easily added to bacteria[115] and lineages of knockout mice with a specific gene’s function disrupted are used to investigate that gene’s function.[116][117] Many organisms have been genetically modified for applications in agriculture, industrial biotechnology, and medicine.

For multicellular organisms, typically the embryo is engineered which grows into the adult genetically modified organism.[118] However, the genomes of cells in an adult organism can be edited using gene therapy techniques to treat genetic diseases.

Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). Molecular Biology of the Cell (Fourth ed.). New York: Garland Science. ISBN978-0-8153-3218-3. A molecular biology textbook available free online through NCBI Bookshelf.

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Nick Bostrom – Wikipedia

Posted: November 21, 2016 at 11:11 am

Nick Bostrom

Nick Bostrom, 2014

Nick Bostrom (English ; Swedish: Niklas Bostrm, IPA:[bustrm]; born 10 March 1973)[1] is a Swedish philosopher at the University of Oxford known for his work on existential risk, the anthropic principle, human enhancement ethics, superintelligence risks, the reversal test, and consequentialism. In 2011, he founded the Oxford Martin Programme on the Impacts of Future Technology,[2] and he is currently the founding director of the Future of Humanity Institute[3] at Oxford University.

He is the author of over 200 publications,[4] including Superintelligence: Paths, Dangers, Strategies (2014), a New York Times bestseller[5] and Anthropic Bias: Observation Selection Effects in Science and Philosophy (2002).[6] In 2009 and 2015, he was included in Foreign Policy’ Top 100 Global Thinkers list.[7][8] Bostrom’s work on superintelligence and his concern for its existential risk to humanity over the coming century has brought both Elon Musk and Bill Gates to similar thinking.[9][10][11]

Bostrom was born in 1973[12] in Helsingborg, Sweden.[4] At a young age, he disliked school, and he ended up spending his last year of high school learning from home. He sought to educate himself in a wide variety of disciplines, including anthropology, art, literature, and science.[13] Despite what has been called a “serious mien”, he once did some turns on London’s stand-up comedy circuit.[4]

He holds a B.A. in philosophy, mathematics, logic and artificial intelligence from the University of Gothenburg and master’s degrees in philosophy and physics, and computational neuroscience from Stockholm University and King’s College London, respectively. During his time at Stockholm University, he researched the relationship between language and reality by studying the analytic philosopher W. V. Quine.[13] In 2000, he was awarded a PhD in philosophy from the London School of Economics. He held a teaching position at Yale University (20002002), and he was a British Academy Postdoctoral Fellow at the University of Oxford (20022005).[6][14]

An important aspect of Bostrom’s research concerns the future of humanity and long-term outcomes.[15][16] He introduced the concept of an existential risk, which he defines as one in which an “adverse outcome would either annihilate Earth-originating intelligent life or permanently and drastically curtail its potential.” In the 2008 volume Global Catastrophic Risks, editors Bostrom and Milan irkovi characterize the relation between existential risk and the broader class of global catastrophic risks, and link existential risk to observer selection effects[17] and the Fermi paradox.[18][19] In a 2013 paper in the journal Global Policy, Bostrom offers a taxonomy of existential risk and proposes a reconceptualization of sustainability in dynamic terms, as a developmental trajectory that minimizes existential risk.[20]

The philosopher Derek Parfit argued for the importance of ensuring the survival of humanity, due to the value of a potentially large number of future generations.[21] Similarly, Bostrom has said that, from a consequentialist perspective, even small reductions in the cumulative amount of existential risk that humanity will face are extremely valuable, to the point where the traditional utilitarian imperativeto maximize expected utilitycan be simplified to the Maxipok principle: maximize the probability of an OK outcome (where an OK outcome is any that avoids existential catastrophe).[22][23]

In 2005, Bostrom founded the Future of Humanity Institute,[13] which researches the far future of human civilization. He is also an adviser to the Centre for the Study of Existential Risk.[16]

In his 2014 book Superintelligence: Paths, Dangers, Strategies, Bostrom reasons that with “cognitive performance greatly [exceeding] that of humans in virtually all domains of interest”, superintelligent agents could promise substantial societal benefits and pose a significant artificial intelligence (AI)-related existential risk. Therefore, it is crucial, he says, that we approach this area with caution, and take active steps to mitigate the risks we face. In January 2015, Bostrom joined Stephen Hawking, Max Tegmark, Elon Musk, Martin Rees, Jaan Tallinn among others, in signing the Future of Life Institute’s open letter warning of the potential dangers of AI. The signatories “…believe that research on how to make AI systems robust and beneficial is both important and timely, and that concrete research should be pursued today.”[24][25]

Bostrom has published numerous articles on anthropic reasoning, as well as the book Anthropic Bias: Observation Selection Effects in Science and Philosophy. In the book, he criticizes previous formulations of the anthropic principle, including those of Brandon Carter, John Leslie, John Barrow, and Frank Tipler.[26]

Bostrom believes that the mishandling of indexical information is a common flaw in many areas of inquiry (including cosmology, philosophy, evolution theory, game theory, and quantum physics). He argues that a theory of anthropics is needed to deal with these. He introduced the Self-Sampling Assumption (SSA) and the Self-Indication Assumption (SIA) and showed how they lead to different conclusions in a number of cases. He pointed out that each is affected by paradoxes or counterintuitive implications in certain thought experiments (the SSA in e.g. the Doomsday argument; the SIA in the Presumptuous Philosopher thought experiment). He suggested that a way forward may involve extending SSA into the Strong Self-Sampling Assumption (SSSA), which replaces “observers” in the SSA definition by “observer-moments”. This could allow for the reference class to be relativized (and he derived an expression for this in the “observation equation”).

In later work, he has described the phenomenon of anthropic shadow, an observation selection effect that prevents observers from observing certain kinds of catastrophes in their recent geological and evolutionary past.[27] Catastrophe types that lie in the anthropic shadow are likely to be underestimated unless statistical corrections are made.

Bostrom is favorable towards “human enhancement”, or “self-improvement and human perfectibility through the ethical application of science”,[28][29] as well as a critic of bio-conservative views.[30] With philosopher Toby Ord, he proposed the reversal test. Given humans’ irrational status quo bias, how can one distinguish between valid criticisms of proposed changes in a human trait and criticisms merely motivated by resistance to change? The reversal test attempts to do this by asking whether it would be a good thing if the trait was altered in the opposite direction.[31]

In 1998, Bostrom co-founded (with David Pearce) the World Transhumanist Association[28] (which has since changed its name to Humanity+). In 2004, he co-founded (with James Hughes) the Institute for Ethics and Emerging Technologies, although he is no longer involved in either of these organisations. Bostrom was named in Foreign Policy’s 2009 list of top global thinkers “for accepting no limits on human potential.”[32]

He has suggested that technology policy aimed at reducing existential risk should seek to influence the order in which various technological capabilities are attained, proposing the principle of differential technological development. This principle states that we ought to retard the development of dangerous technologies, particularly ones that raise the level of existential risk, and accelerate the development of beneficial technologies, particularly those that protect against the existential risks posed by nature or by other technologies.

Bostrom’s simulation argument posits that at least one of the following statements is very likely to be true:

To estimate the probability of at least one of those propositions holding, he offers the following equation:[33]

where:

N can be calculated by multiplying the fraction of civilizations interested in performing such simulations ( f 1 {displaystyle f_{textrm {1}}} ) by the number of simulations run by such civilizations ( N 1 {displaystyle N_{textrm {1}}} ):

N = f 1 {displaystyle N=f_{textrm {1}}} N 1 {displaystyle N_{textrm {1}}}

Thus the formula becomes:

Because post-human computing power N 1 {displaystyle N_{textrm {1}}} will be such a large value, at least one of the following three approximations will be true:

Bostrom has provided policy advice and consulted for an extensive range of governments and organisations. He gave evidence to the House of Lords, Select Committee on Digital Skills, with Anders Sandberg, he was a consultant to the UK Government Office for Science (GOSE) and Foresight for “The Future of Human Identity” report and an Expert Member for World Economic Forum’s Agenda Council for Catastrophic Risks. He is an advisory board member for the Machine Intelligence Research Institute, Future of Life Institute, Foundational Questions Institute In Physics and Cosmology and an external advisor for the Cambridge Centre for the Study of Existential Risk.[34]

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The Art Of Memetics: Edward Wilson, Wes Unruh, Ray Carney …

Posted: at 11:07 am

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The Art Of Memetics: Edward Wilson, Wes Unruh, Ray Carney …

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Neurotechnology: Premises, Potential, and Problems …

Posted: November 12, 2016 at 5:25 pm

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New technologies that allow us to investigate mechanisms and functions of the brain have shown considerable promise in treating brain disease and injury. These emerging technologies also provide a means to assess and manipulate human consciousness, cognitions, emotions, and behaviors, bringing with them the potential to transform society. Neurotechnology: Premises, Potential, and Problems explores the technical, moral, legal, and sociopolitical issues that arise in and from todays applications of neuroscience and technology and discusses their implications for the future.

Some of the issues raised in this thought-provoking volume include:

With contributions from an international group of experts working on the cutting edge of neurotechnology, this volume lays the groundwork to appreciate the ethical, legal, and social aspects of the science in ways that keep pace with this rapidly progressing field.

Scientific and Philosophical Perspectives in Neuroethics

James J. Giordano

Paperback

$62.00 Prime

James Giordano, PhD, is Director of the Center for Neurotechnology Studies at the Potomac Institute for Policy Studies, Arlington, Virginia, Fulbright Professor of Neuroscience, Neurotechnology and Ethics at the Human Science Center of Ludwig-Maximilians University, Munich, Germany, and Research Professor of Neurosciences and Ethics in the Department of Electrical and Computational Engineering at the University of New Mexico in Albuquerque. His ongoing research addresses the ethical issues that are generated from neuroscientific and neurotechnological research and its applications in medicine, public life, and sociocultural conduct.

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Genetic Engineering | MSPCA-Angell

Posted: November 10, 2016 at 5:32 pm

The MSPCAbelieves scientists ability to clone animals, to alter the genetic makeup of an animal, and to transfer pieces of genetic material from one species to another raises serious concerns for animals and humans alike.

This pagewill explore issues related to genetic engineering, transgenic animals, and cloned animals. It will examine the implications of genetic engineering on human and animal welfare and will touch on some related moral and ethical concerns that our society has so far failed to completely address.

Definitions

Problems related to the physical and psychological well-being of cloned and transgenic animals, significant ethical concerns about the direct manipulation of genetic material, and questions about the value of life itself must all be carefully weighed against the potential benefits of genetic engineering for disease research, agricultural purposes, vaccine development, pharmaceutical products, and organ transplants.

Genetic engineering is, as yet, an imperfect science that yields imperfect results.

Changes in animal growth and development brought about by genetic engineering and cloning are less predictable, more rapid, and often more debilitating than changes brought about through the traditional process of selective breeding.

This is especially apparent with cloning. Success rates are incredibly low; on average, less than 5% of cloned embryos are born and survive.

Clones are created at a great cost to animals. The clones that are successful, as well as those that do not survive and the surrogates who carry them, suffer greatly.Many of the cloned animals that do survive are plagued by severe health problems.

Offspring suffer from severe birth defects such as Large Offspring Syndrome (LOS), in which the cloned offspring are significantly larger than normal fetuses; hydrops, a typically fatal condition in which the mother or the fetus swells with fluid; respiratory distress; developmental problems; malformed organs; musculoskeletal deformities; or weakened immune systems, to name only a few.

Additionally, surrogates are subjected to repeated invasive procedures to harvest their eggs, implant embryos, or due to the offsprings birth defects surgical intervention to deliver their offspring. All of these problems occur at much higher rates than for offspring produced via traditional breeding methods.

Cloning increases existing animal welfare and environmental concerns related to animal agriculture.

In 1996, the birth of the ewe, Dolly, marked the first successful cloning of a mammal from adult cells. At the time of her birth, the researchers who created Dolly acknowledged the inefficiency of the new technology: it took 277 attempts to create this one sheep, and of these, only 29 early embryos developed, and an even smaller number of these developed into live fetuses. In the end, Dolly was the sole surviving clone. She was euthanized in 2003 at just 6 years of age, about half as old as sheep are expected to live, and with health problems more common in older sheep.

Since Dollys creation, the process of cloning has not demonstrated great improvement in efficiency or rates of success. A 2003 review of cloning in cattle found that less than 5% of cloned embryos transferred into surrogate cows survived; a 2016 study showedno noticeable increase in efficiency, with the success rate being about 1%.

Currently, research is focused on cloning for agricultural purposes. Used alone, or in concert with genetic engineering, the objective is to clone the best stock to reproduce whole herds or flocks with desired uniform characteristics of a specific trait, such as fast growth, leaner meat, or higher milk production. Cloning is often pursued to produce animals that grow faster so they can be slaughtered sooner and to raise more animals in a smaller space.

For example, transgenic fish are engineered to grow larger at a faster rate and cows injected with genetically engineered products to increase their productivity. Another example of this is the use of the genetically engineered drug, bovine growth hormone (BGH or BST) to increase milk production in dairy cows. This has also been associated with increased cases of udder disease, spontaneous abortion, lameness, and shortened lifespan. The use of BGH is controversial; many countries (such as Canada, Japan, Australia, and countries in the EU) do not allow it, and many consumers try to avoid it.A rise in transgenic animals used for agriculture will only exacerbate current animal welfare and environmental concerns with existing intensive farming operations.(For more information on farming and animal welfare, visit the MSPCAs Farm Animal Welfare page.)

Much remains unknown about thepotential environmental impacts of widespread cloning of animals. The creation of genetically identical animals leads to concerns about limited agricultural animal gene pools. The effects of creating uniform herds of animals and the resulting loss of biodiversity, have significant implications for the environment and for the ability of cloned herds to withstand diseases. This could make an impact on the entireagriculture industry and human food chain.

These issues became especiallyconcerning when, in 2008, the Federal Drug Administration not only approved the sale of meat from the offspring of cloned animals, but also did not require that it be labeled as such. There have been few published studies that examine the composition of milk, meat, or eggs from cloned animals or their progeny, including the safety of eating those products. The health problems associated with cloned animals, particularly those that appear healthy but have concealed illnesses or problems that appear unexpectedly later in life, could potentially pose risks to the safety of the food products derived from those animals.

Genetically Engineered Pets

Companion animals have also been cloned. The first cloned cat, CC, was created in 2001. CCs creation marked the beginning of the pet cloning industry, in which pet owners could pay to bank DNA from their companion dogs and cats to be cloned in the future. In 2005, the first cloned dog was created; later, the first commercially cloned dog followed at a cost of $50,000. Many consumers assume that cloning will produce a carbon copy of their beloved pet, but this is not the case. Even though the animals are genetically identical, they often do not resemble each other physically or behaviorally.

To date, the pet cloning industry has not been largely successful. However, efforts to make cloning a successful commercial venture are still being put forth.RBio (formerly RNL Bio), a Korean biotechnology company, planned to create a research center that would produce 1,000 cloned dogs annually by 2013. However, RBio, considered a black market cloner, failed to make any significant strides in itscloning endeavors and seems to have been replaced by other companies, such as South Korean-based Sooam Biotech, now the worlds leader in commercial pet cloning. Since 2006, Sooam has cloned over 800 dogs, in addition to other animals, such as cattle and pigs, for breed preservation and medical research.

While South Korean animal cloning expands, the interest in companion animal cloning in the United States continues to remain low. In 2009, the American company BioArts ceased its dog cloning services and ended its partnership with Sooam, stating in a press release that cloning procedures were still underdeveloped and that the cloning market itself was weak and unethical. Companion animal cloning causes concern not only because of the welfare issues inherent in the cloning process, but also because of its potential to contribute to pet overpopulation problem in the US, as millions of animals in shelters wait for homes.

Cloning and Medical Research

Cloning is also used to produce copies of transgenic animals that have been created to mimic certain human diseases. The transgenic animals are created, then cloned, producing a supply of animals for biomedical testing.

A 1980 U.S. Supreme Court decision to permit the patenting of a microorganism that could digest crude oil had a great impact on animal welfare and genetic engineering. Until that time, the U.S. Patent Office had prohibited the patenting of living organisms. However, following the Supreme Court decision, the Patent Office interpreted this ruling to extend to the patenting of all higher life forms, paving the way for a tremendous explosion of corporate investment in genetic engineering research.

In 1988, the first animal patent was issued to Harvard University for the Oncomouse, a transgenic mouse genetically modified to be more prone to develop cancers mimicking human disease. Since then, millions of transgenic mice have been produced. Transgenic rats, rabbits, monkeys, fish, chickens, pigs, sheep, goats, cows, horses, cats, dogs, and other animals have also been created.

Both expected and unexpected results occur in the process of inserting new genetic material into an egg cell. Defective offspring can suffer from chromosomal abnormalities that can cause cancer, fatal bleeding disorders, inability to reproduce, early uterine death, lack of ability to nurse, and such diseases as arthritis, diabetes, liver disease, and kidney disease.

The production of transgenic animals is of concern because genetic engineering is often used to create animals with diseases that cause intense suffering. Among the diseases that can be produced in genetically engineered research mice are diabetes, cancer, cystic fibrosis, sickle-cell anemia, Huntingtons disease, Alzheimers disease, and a rare but severe neurological condition called Lesch-Nyhansyndromethat causes the sufferer to self-mutilate. Animals carrying the genes for these diseases can suffer for long periods of time, both in the laboratory and while they are kept on the shelf by laboratory animal suppliers.

Another reason for the production of transgenic animals is pharming, in which sheep and goats are modified to produce pharmaceuticals in their milk. In 2009, the first drug produced by genetically engineered animals was approved by the FDA. The drug ATryn, used to prevent fatal blood clots in humans, is derived from goats into which a segment of human DNA has been inserted, causing them to produce an anticoagulant protein in their milk. This marks the first time a drug has been manufactured from a herd of animals created specifically to produce a pharmaceutical.

A company has also manufactured a drug produced in the milk of transgenic rabbits to treat a dangerous tissue swelling caused by a human protein deficiency. Yet another pharmaceutical manufacturer, PharmAnthene, was funded by the US Department of Defense to develop genetically engineered goats whose milk produces proteins used in a drug to treat nerve gas poisoning. The FDA also approved a drug whose primary proteins are also found in the milk of genetically engineered goats, who are kept at a farm in Framingham, Massachusetts. Additionally, a herd of cattle was recently developed that produces milk containing proteins that help to treat human emphysema. These animals are essentially used as pharmaceutical-production machines to manufacture only those substances they were genetically modified to produce; they are not used as part of the normal food supply chain for items such as meat or milk.

The transfer of animal tissues from one species to another raises potentially serious health issues for animals and humans alike.

Some animals are also genetically modified to produce tissues and organs to be used for human transplant purposes (xenotransplantation). Much effort is being focused in this area as the demand for human organs for transplantation far exceeds the supply, with pigs the current focus of this research. While efforts to date have been hampered by a pig protein that can cause organ rejection by the recipients immune system, efforts are underway to develop genetically modified swine with a human protein that would mitigate the chance of organ rejection.

Little is known about the ways in which diseases can be spread from one species to another, raising concerns for both animals and people, and calling into question the safety of using transgenic pigs to supply organs for human transplant purposes. Scientists have identified various viruses common in the heart, spleen, and kidneys of pigs that could infect human cells. In addition, new research is shedding light on particles called prions that, along with viruses and bacteria, may transmit fatal diseases between animals and from animals to humans.

Acknowledging the potential for transmission of viruses from animals to humans, the National Institutes of Health, a part of the U.S. Department of Health and Human Services,issued a moratorium in 2015 onxenotransplantation until the risks are better understood, ceasing funding until more research has been carried out. With the science of genetic engineering, the possibilities are endless, but so too are the risks and concerns.

Genetic engineering research has broad ethical and moral ramifications with few established societal guidelines.

While biotechnology has been quietly revolutionizing the science for decades, public debate in the United Statesover the moral, ethical, and physical effects of this research has been insufficient. To quote Colorado State University Philosopher Bernard Rollin, We cannot control technology if we do not understand it, and we cannot understand it without a careful discussion of the moral questions to which it gives rise.

Research into non-animal methods of achieving some of the same goals looks promising.

Researchers in the U.S. and elsewhere have found ways togenetically engineer cereal grains to produce human proteins. One example of this, developed in the early 2000s, is a strain of rice that can produce a human protein used to treat cystic fibrosis. Wheat, corn, and barley may also be able to be used in similar ways at dramatically lower financial and ethical costs than genetically engineering animals for this purpose.

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Darwinism – Wikipedia

Posted: November 6, 2016 at 7:06 pm

Darwinism is a theory of biological evolution developed by the English naturalist Charles Darwin (1809-1882) and others, stating that all species of organisms arise and develop through the natural selection of small, inherited variations that increase the individual’s ability to compete, survive, and reproduce. Also called Darwinian theory, it originally included the broad concepts of transmutation of species or of evolution which gained general scientific acceptance after Darwin published On the Origin of Species in 1859, including concepts which predated Darwin’s theories, but subsequently referred to specific concepts of natural selection, of the Weismann barrier or in genetics of the central dogma of molecular biology.[1] Though the term usually refers strictly to biological evolution, creationists have appropriated it to refer to the origin of life, and it has even been applied to concepts of cosmic evolution, both of which have no connection to Darwin’s work. It is therefore considered the belief and acceptance of Darwin’s and of his predecessors’ workin place of other theories, including divine design and extraterrestrial origins.[2][3]

English biologist Thomas Henry Huxley coined the term Darwinism in April 1860.[4] It was used to describe evolutionary concepts in general, including earlier concepts published by English philosopher Herbert Spencer. Many of the proponents of Darwinism at that time, including Huxley, had reservations about the significance of natural selection, and Darwin himself gave credence to what was later called Lamarckism. The strict neo-Darwinism of German evolutionary biologist August Weismann gained few supporters in the late 19th century. During the approximate period of the 1880s to about 1920, sometimes called “the eclipse of Darwinism,” scientists proposed various alternative evolutionary mechanisms which eventually proved untenable. The development of the modern evolutionary synthesis from the 1930s to the 1950s, incorporating natural selection with population genetics and Mendelian genetics, revived Darwinism in an updated form.[5]

While the term Darwinism has remained in use amongst the public when referring to modern evolutionary theory, it has increasingly been argued by science writers such as Olivia Judson and Eugenie Scott that it is an inappropriate term for modern evolutionary theory.[6][7] For example, Darwin was unfamiliar with the work of the Moravian scientist and Augustinian friar Gregor Mendel,[8] and as a result had only a vague and inaccurate understanding of heredity. He naturally had no inkling of later theoretical developments and, like Mendel himself, knew nothing of genetic drift, for example.[9][10] In the United States, creationists often use the term “Darwinism” as a pejorative term in reference to beliefs such as scientific materialism, but in the United Kingdom the term has no negative connotations, being freely used as a shorthand for the body of theory dealing with evolution, and in particular, with evolution by natural selection.[6]

While the term Darwinism had been used previously to refer to the work of Erasmus Darwin in the late 18th century, the term as understood today was introduced when Charles Darwin’s 1859 book On the Origin of Species was reviewed by Thomas Henry Huxley in the April 1860 issue of the Westminster Review.[12] Having hailed the book as “a veritable Whitworth gun in the armoury of liberalism” promoting scientific naturalism over theology, and praising the usefulness of Darwin’s ideas while expressing professional reservations about Darwin’s gradualism and doubting if it could be proved that natural selection could form new species,[13] Huxley compared Darwin’s achievement to that of Nicolaus Copernicus in explaining planetary motion:

What if the orbit of Darwinism should be a little too circular? What if species should offer residual phenomena, here and there, not explicable by natural selection? Twenty years hence naturalists may be in a position to say whether this is, or is not, the case; but in either event they will owe the author of “The Origin of Species” an immense debt of gratitude…. And viewed as a whole, we do not believe that, since the publication of Von Baer’s “Researches on Development,” thirty years ago, any work has appeared calculated to exert so large an influence, not only on the future of Biology, but in extending the domination of Science over regions of thought into which she has, as yet, hardly penetrated.[4]

Another important evolutionary theorist of the same period was the Russian geographer and prominent anarchist Peter Kropotkin who, in his book Mutual Aid: A Factor of Evolution (1902), advocated a conception of Darwinism counter to that of Huxley. His conception was centred around what he saw as the widespread use of co-operation as a survival mechanism in human societies and animals. He used biological and sociological arguments in an attempt to show that the main factor in facilitating evolution is cooperation between individuals in free-associated societies and groups. This was in order to counteract the conception of fierce competition as the core of evolution, which provided a rationalisation for the dominant political, economic and social theories of the time; and the prevalent interpretations of Darwinism, such as those by Huxley, who is targeted as an opponent by Kropotkin. Kropotkin’s conception of Darwinism could be summed up by the following quote:

In the animal world we have seen that the vast majority of species live in societies, and that they find in association the best arms for the struggle for life: understood, of course, in its wide Darwinian sensenot as a struggle for the sheer means of existence, but as a struggle against all natural conditions unfavourable to the species. The animal species, in which individual struggle has been reduced to its narrowest limits, and the practice of mutual aid has attained the greatest development, are invariably the most numerous, the most prosperous, and the most open to further progress. The mutual protection which is obtained in this case, the possibility of attaining old age and of accumulating experience, the higher intellectual development, and the further growth of sociable habits, secure the maintenance of the species, its extension, and its further progressive evolution. The unsociable species, on the contrary, are doomed to decay.[14]

Peter Kropotkin, Mutual Aid: A Factor of Evolution (1902), Conclusion

“Darwinism” soon came to stand for an entire range of evolutionary (and often revolutionary) philosophies about both biology and society. One of the more prominent approaches, summed in the 1864 phrase “survival of the fittest” by Herbert Spencer, later became emblematic of Darwinism even though Spencer’s own understanding of evolution (as expressed in 1857) was more similar to that of Jean-Baptiste Lamarck than to that of Darwin, and predated the publication of Darwin’s theory in 1859. What is now called “Social Darwinism” was, in its day, synonymous with “Darwinism”the application of Darwinian principles of “struggle” to society, usually in support of anti-philanthropic political agenda. Another interpretation, one notably favoured by Darwin’s half-cousin Francis Galton, was that “Darwinism” implied that because natural selection was apparently no longer working on “civilized” people, it was possible for “inferior” strains of people (who would normally be filtered out of the gene pool) to overwhelm the “superior” strains, and voluntary corrective measures would be desirablethe foundation of eugenics.

In Darwin’s day there was no rigid definition of the term “Darwinism,” and it was used by opponents and proponents of Darwin’s biological theory alike to mean whatever they wanted it to in a larger context. The ideas had international influence, and Ernst Haeckel developed what was known as Darwinismus in Germany, although, like Spencer’s “evolution,” Haeckel’s “Darwinism” had only a rough resemblance to the theory of Charles Darwin, and was not centered on natural selection.[15] In 1886, Alfred Russel Wallace went on a lecture tour across the United States, starting in New York and going via Boston, Washington, Kansas, Iowa and Nebraska to California, lecturing on what he called “Darwinism” without any problems.[16]

In his book Darwinism (1889), Wallace had used the term pure-Darwinism which proposed a “greater efficacy” for natural selection.[17][18]George Romanes dubbed this view as “Wallaceism”, noting that in contrast to Darwin, this position was advocating a “pure theory of natural selection to the exclusion of any supplementary theory.”[19][20] Taking influence from Darwin, Romanes was a proponent of both natural selection and the inheritance of acquired characteristics. The latter was denied by Wallace who was a strict selectionist.[21] Romanes’ definition of Darwinism conformed directly with Darwin’s views and was contrasted with Wallace’s definition of the term.[22]

The term Darwinism is often used in the United States by promoters of creationism, notably by leading members of the intelligent design movement, as an epithet to attack evolution as though it were an ideology (an “ism”) of philosophical naturalism, or atheism.[23] For example, UC Berkeley law professor and author Phillip E. Johnson makes this accusation of atheism with reference to Charles Hodge’s book What Is Darwinism? (1874).[24] However, unlike Johnson, Hodge confined the term to exclude those like American botanist Asa Gray who combined Christian faith with support for Darwin’s natural selection theory, before answering the question posed in the book’s title by concluding: “It is Atheism.”[25][26] Creationists use the term Darwinism, often pejoratively, to imply that the theory has been held as true only by Darwin and a core group of his followers, whom they cast as dogmatic and inflexible in their belief.[27] In the 2008 documentary film Expelled: No Intelligence Allowed, which promotes intelligent design (ID), American writer and actor Ben Stein refers to scientists as Darwinists. Reviewing the film for Scientific American, John Rennie says “The term is a curious throwback, because in modern biology almost no one relies solely on Darwin’s original ideas… Yet the choice of terminology isn’t random: Ben Stein wants you to stop thinking of evolution as an actual science supported by verifiable facts and logical arguments and to start thinking of it as a dogmatic, atheistic ideology akin to Marxism.” [28]

However, Darwinism is also used neutrally within the scientific community to distinguish the modern evolutionary synthesis, sometimes called “neo-Darwinism,” from those first proposed by Darwin. Darwinism also is used neutrally by historians to differentiate his theory from other evolutionary theories current around the same period. For example, Darwinism may be used to refer to Darwin’s proposed mechanism of natural selection, in comparison to more recent mechanisms such as genetic drift and gene flow. It may also refer specifically to the role of Charles Darwin as opposed to others in the history of evolutionary thoughtparticularly contrasting Darwin’s results with those of earlier theories such as Lamarckism or later ones such as the modern evolutionary synthesis.

In political discussions in the United States, the term is mostly used by its enemies. “It’s a rhetorical device to make evolution seem like a kind of faith, like ‘Maoism,'” says Harvard University biologist E. O. Wilson. He adds, “Scientists don’t call it ‘Darwinism’.”[29] In the United Kingdom the term often retains its positive sense as a reference to natural selection, and for example British ethologist and evolutionary biologist Richard Dawkins wrote in his collection of essays A Devil’s Chaplain, published in 2003, that as a scientist he is a Darwinist.[30]

In his 1995 book Darwinian Fairytales, Australian philosopher David Stove[31] used the term “Darwinism” in a different sense than the above examples. Describing himself as non-religious and as accepting the concept of natural selection as a well-established fact, Stove nonetheless attacked what he described as flawed concepts proposed by some “Ultra-Darwinists.” Stove alleged that by using weak or false ad hoc reasoning, these Ultra-Darwinists used evolutionary concepts to offer explanations that were not valid (e.g., Stove suggested that sociobiological explanation of altruism as an evolutionary feature was presented in such a way that the argument was effectively immune to any criticism). Philosopher Simon Blackburn wrote a rejoinder to Stove,[32] though a subsequent essay by Stove’s protegee James Franklin’s[33] suggested that Blackburn’s response actually “confirms Stove’s central thesis that Darwinism can ‘explain’ anything.”

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Darwinism – Wikipedia

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