Barbara McClintock

Barbara McClintock (June 16, 1902 – September 2, 1992) was an American scientist and cytogeneticist who was awarded the 1983 Nobel Prize in Physiology or Medicine. McClintock received her PhD in botany from Cornell University in 1927. There she started her career as the leader in the development of maize cytogenetics, the focus of her […]

Barbara McClintock (June 16, 1902 – September 2, 1992) was an American scientist and cytogeneticist who was awarded the 1983 Nobel Prize in Physiology or Medicine. McClintock received her PhD in botany from Cornell University in 1927. There she started her career as the leader in the development of maize cytogenetics, the focus of her research for the rest of her life. From the late 1920s, McClintock studied chromosomes and how they change during reproduction in maize. She developed the technique for visualizing maize chromosomes and used microscopic analysis to demonstrate many fundamental genetic ideas. One of those ideas was the notion of genetic recombination by crossing-over during meiosis—a mechanism by which chromosomes exchange information. She produced the first genetic map for maize, linking regions of the chromosome to physical traits. She demonstrated the role of the telomere and centromere, regions of the chromosome that are important in the conservation of genetic information. She was recognized among the best in the field, awarded prestigious fellowships, and elected a member of the National Academy of Sciences in 1944.

During the 1940s and 1950s, McClintock discovered transposition and used it to demonstrate that genes are responsible for turning physical characteristics on and off. She developed theories to explain the suppression and expression of genetic information from one generation of maize plants to the next. Due to skepticism of her research and its implications, she stopped publishing her data in 1953.

Later, she made an extensive study of the cytogenetics and ethnobotany of maize races from South America. McClintock’s research became well understood in the 1960s and 1970s, as other scientists confirmed the mechanisms of genetic change and genetic regulation that she had demonstrated in her maize research in the 1940s and 1950s. Awards and recognition for her contributions to the field followed, including the Nobel Prize in Physiology or Medicine, awarded to her in 1983 for the discovery of genetic transposition; she is the only woman to receive an unshared Nobel Prize in that category.[1]

Epigenetics

Epigenetics (from Ancient Greek επί/epi = ‘upon’, ‘over’, ‘above’ and γενετικός/genetikos = ‘genitive’ > γενεά/genea = ‘generation’ > γεννώ/geno = ‘birth to’ > γένεσις/genesis = ‘origin’) is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external orenvironmental factors that switch genes on and off and […]

Epigenetics (from Ancient Greek ???/epi = ‘upon’, ‘over’, ‘above’ and ?????????/genetikos = ‘genitive’ > ?????/genea = ‘generation’ > ?????/geno = ‘birth to’ > ???????/genesis = ‘origin’) is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external orenvironmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence.[1][2] Hence, epigenetic research seeks to describe dynamic alterations in the transcriptional potential of a cell. These alterations may or may not be heritable, although the use of the term “epigenetic” to describe processes that are not heritable is controversial.[3] Unlike genetics based on changes to the DNA sequence (the genotype), the changes in gene expression or cellular phenotype of epigenetics have other causes, thus use of the prefix epi-(Greek: ???– over, outside of, around).[4][5]

The term also refers to the changes themselves: functionally relevant changes to the genome that do not involve a change in the nucleotide sequence. Examples of mechanisms that produce such changes are DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA. These epigenetic changes may last through cell divisions for the duration of the cell’s life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism;[6] instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.[7]

One example of an epigenetic change in eukaryotic biology is the process of cellular differentiation. During morphogenesis, totipotent stem cells become the various pluripotentcell lines of the embryo, which in turn become fully differentiated cells. In other words, as a single fertilized egg cell – the zygote – continues to divide, the resulting daughter cells change into all the different cell types in an organism, including neurons, muscle cells, epithelium, endothelium of blood vessels, etc., by activating some genes while inhibiting the expression of others.[8]

Chimpanzee Genome Project

The Chimpanzee Genome Project is an effort to determine the DNA sequence of the Chimpanzee genome. It is expected that by comparing the genomes of humans and other apes, it will be possible to better understand what makes humans distinct from other species from a genetic perspective. Human and chimpanzee chromosomes are very similar. The […]

The Chimpanzee Genome Project is an effort to determine the DNA sequence of the Chimpanzee genome. It is expected that by comparing the genomes of humans and other apes, it will be possible to better understand what makes humans distinct from other species from a genetic perspective.

Human and chimpanzee chromosomes are very similar. The primary difference is that humans have one fewer pair of chromosomes than do other great apes. Humans have 23 pairs of chromosomes and other great apes have 24 pairs of chromosomes. In the human evolutionary lineage, two ancestral ape chromosomes fused at their telomeres, producing human chromosome 2.[3] There are nine other major chromosomal differences between chimpanzees and humans: chromosome segment inversions on human chromosomes 1, 4, 5, 9,12, 15, 16, 17, and 18. After the completion of the Human genome project, a common chimpanzee genome project was initiated. In December 2003, a preliminary analysis of 7600 genes shared between the two genomes confirmed that certain genes such as theforkhead-box P2 transcription factor, which is involved in speech development, are different in the human lineage. Several genes involved in hearing were also found to have changed during human evolution, suggesting selection involving human language-related behavior. Differences between individual humans and common chimpanzees are estimated to be about 10 times the typical difference between pairs of humans.[4]

About 600 genes have been identified that may have been undergoing strong positive selection in the human and chimp lineages; many of these genes are involved in immune system defense against microbial disease (example: granulysin is protective against Mycobacterium tuberculosis [8]) or are targeted receptors of pathogenic microorganisms (example: Glycophorin C and Plasmodium falciparum). By comparing human and chimp genes to the genes of other mammals, it has been found that genes coding fortranscription factors, such as forkhead-box P2 (FOXP2), have often evolved faster in the human relative to chimp; relatively small changes in these genes may account for the morphological differences between humans and chimps. A set of 348 transcription factor genes code for proteins with an average of about 50 percent more amino acid changes in the human lineage than in the chimp lineage.

Six human chromosomal regions were found that may have been under particularly strong and coordinated selection during the past 250,000 years. These regions contain at least one marker allele that seems unique to the human lineage while the entire chromosomal region shows lower than normal genetic variation. This pattern suggests that one or a few strongly selected genes in the chromosome region may have been preventing the random accumulation of neutral changes in other nearby genes. One such region on chromosome 7 contains the FOXP2 gene (mentioned above) and this region also includes the Cystic fibrosis transmembrane conductance regulator (CFTR) gene, which is important for ion transport in tissues such as the salt-secreting epithelium of sweat glands. Human mutations in the CFTR gene might be selected for as a way to survivecholera.[9]

Another such region on chromosome 4 may contain elements regulating the expression of a nearby protocadherin gene that may be important for brain development and function. Although changes in expression of genes that are expressed in the brain tend to be less than for other organs (such as liver) on average, gene expression changes in the brain have been more dramatic in the human lineage than in the chimp lineage.[10] This is consistent with the dramatic divergence of the unique pattern of human brain development seen in the human lineage compared to the ancestral great ape pattern. The protocadherin-beta gene cluster on chromosome 5 also shows evidence of possible positive selection.[11]

Results from the human and chimp genome analyses should help in understanding some human diseases. Humans appear to have lost a functional caspase-12 gene, which in other primates codes for an enzyme that may protect against Alzheimer’s disease.

The results of the chimpanzee genome project suggest that when ancestral chromosomes 2A and 2B fused to produce human chromosome 2, no genes were lost from the fused ends of 2A and 2B. At the site of fusion, there are approximately 150,000 base pairs of sequence not found in chimpanzee chromosomes 2A and 2B. Additional linked copies of the PGML/FOXD/CBWD genes exist elsewhere in the human genome, particularly near the p end of chromosome 9. This suggests that a copy of these genes may have been added to the end of the ancestral 2A or 2B prior to the fusion event. It remains to be determined if these inserted genes confer a selective advantage.

  • PGML. The phosphoglucomutase-like gene of human chromosome 2. This gene is incomplete and may not produce a functional transcript.[12]
  • FOXD. The forkhead box D4-like gene is an example of an intronless gene. The function of this gene is not known, but it may code for a transcription control protein.
  • CBWD. Cobalamin synthetase is a bacterial enzyme that makes vitamin B12. In the distant past, a common ancestor to mice and apes incorporated a copy of a cobalamin synthetase gene (see: Horizontal gene transfer). Humans are unusual in that they have several copies of cobalamin synthetase-like genes, including the one on chromosome 2. It remains to be determined what the function of these human cobalamin synthetase-like genes is. If these genes are involved in vitamin B12 metabolism, this could be relevant to human evolution. A major change in human development is greater post-natal brain growth than is observed in other apes. Vitamin B12is important for brain development, and vitamin B12 deficiency during brain development results in severe neurological defects in human children.
  • CXYorf1-like protein. Several transcripts of unknown function corresponding to this region have been isolated. This region is also present in the closely related chromosome 9p terminal region that contains copies of the PGML/FOXD/CBWD genes.
  • Many ribosomal protein L23a pseudogenes are scattered through the human genome.

Benzodiazepines (BZD)

Benzodiazepines (BZD), sometimes called “benzos“, are a class of psychoactive drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. The first such drug, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955, and made available in 1960 by Hoffmann–La Roche – which, since 1963, has also marketed […]

Benzodiazepines (BZD), sometimes called “benzos“, are a class of psychoactive drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. The first such drug, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955, and made available in 1960 by Hoffmann–La Roche – which, since 1963, has also marketed the benzodiazepinediazepam (Valium).[1] In 1977 benzodiazepines were globally the most prescribed medications.[2]

Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting insedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties. High doses of many shorter-acting benzodiazepines may also cause anterograde amnesia and dissociation.[3] These properties make benzodiazepines useful in treating anxiety, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal and as a premedication for medical or dental procedures.[4] Benzodiazepines are categorized as either short-, intermediate-, or long-acting. Short- and intermediate-acting benzodiazepines are preferred for the treatment of insomnia; longer-acting benzodiazepines are recommended for the treatment of anxiety.[5]

Benzodiazepines are generally viewed as safe and effective for short-term use, although cognitive impairment and paradoxical effects such as aggression or behavioral disinhibition occasionally occur. A minority of people can have paradoxical reactions such as worsened agitation or panic.[6] Long-term use is controversial because of concerns about adverse psychological and physical effects, decreasing effectiveness, and physical dependence and withdrawal.[7][8] As a result of adverse effects associated with the long-term use of benzodiazepines, withdrawal from benzodiazepines, in general, leads to improved physical and mental health.[9][10]The elderly are at an increased risk of suffering from both short- and long-term adverse effects,[9][11] and as a result, all benzodiazepines are listed in the Beers List of inappropriate medications for older adults.[12]

There is controversy concerning the safety of benzodiazepines in pregnancy. While they are not major teratogens, uncertainty remains as to whether they cause cleft palate in a small number of babies and whether neurobehavioural effects occur as a result of prenatal exposure;[13] they are known to cause withdrawal symptoms in the newborn. Benzodiazepines can be taken in overdoses and can cause dangerous deep unconsciousness. However, they are much less toxic than their predecessors, the barbiturates, and death rarely results when a benzodiazepine is the only drug taken; however, when combined with other central nervous system (CNS) depressants such as ethanol and opioids, the potential for toxicity and fatal overdose increases.[14] Benzodiazepines are commonly misused and taken in combination with other drugs of abuse.[15][16][17]

cells

A eukaryote (/juːˈkæri.oʊt/ or /juːˈkæriət/ yoo-karr-ee-oht or yoo-karr-ee-ət) is any organism whose cells contain a nucleus and other organelles enclosed within membranes. Eukaryotes belong to the taxon Eukarya or Eukaryota. The defining feature that sets eukaryotic cells apart from prokaryotic cells (Bacteria and Archaea) is that they have membrane-bound organelles, especially the nucleus, which contains the […]

A eukaryote (/ju??kæri.o?t/ or /ju??kæri?t/ yoo-karr-ee-oht or yoo-karr-ee-?t) is any organism whose cells contain a nucleus and other organelles enclosed within membranes.

Eukaryotes belong to the taxon Eukarya or Eukaryota. The defining feature that sets eukaryotic cells apart from prokaryotic cells (Bacteria and Archaea) is that they have membrane-bound organelles, especially the nucleus, which contains the genetic material, and is enclosed by the nuclear envelope.[2][3][4] The presence of a nucleus gives eukaryotes their name, which comes from the Greek?? (eu, “well”) and ?????? (karyon, “nut” or “kernel”).[5] Eukaryotic cells also contain other membrane-bound organelles such asmitochondria and the Golgi apparatus. In addition, plants and algae contain chloroplasts. Eukaryotic organisms may be unicellular, ormulticellular. Only eukaryotes have many kinds of tissue made up of different cell types.

Eukaryotes can reproduce both by asexual reproduction through mitosis and sexual reproduction through meiosis. In mitosis, one cell divides to produce two genetically identical cells. In meiosis, DNA replication is followed by two rounds of cell division to produce four daughter cells each with half the number of chromosomes as the original parent cell (haploid cells). These act as sex cells (gametes – each gamete has just one complement of chromosomes, each a unique mix of the corresponding pair of parental chromosomes) resulting from genetic recombination during meiosis.

The domain Eukaryota appears to be monophyletic, and so makes up one of the three domains of life. The two other domains,Bacteria and Archaea, are prokaryotes and have none of the above features. Eukaryotes represent a tiny minority of all living things;[6]even the cells in a human’s body are outnumbered ten to one by bacteria in the gut.[7][8] However, due to their much larger size, eukaryotes’ collective worldwide biomass is estimated at about equal to that of prokaryotes.[6] Eukaryotes first developed approximately 1.6–2.1 billion years ago.

A prokaryote is a single-celled organism that lacks a membrane-bound nucleus (karyon), mitochondria, or any other membrane-bound organelle.[1] The word prokaryote comes from the Greek ??? (pro) “before” and ?????? (karyon) “nut orkernel“.[2][3] Prokaryotes can be divided into two domains, Archaea and Bacteria. Species with nuclei and organelles are placed in the domain Eukaryota.[4]

In the prokaryotes all the intracellular water-soluble components (proteins, DNA and metabolites) are located together in thecytoplasm enclosed by the cell membrane, rather than in separate cellular compartments. Bacteria, however, do possess protein-based bacterial microcompartments, which are thought to act as primitive organelles enclosed in protein shells.[5][6]Some prokaryotes, such as cyanobacteria may form large colonies. Others, such as myxobacteria, have multicellular stages in their life cycles.[7]

Molecular studies have provided insight into the evolution and interrelationships of the three domains of biological species.[8]Eukaryotes are organisms, including humans, whose cells have a well defined membrane-bound nucleus (containing chromosomal DNA) and organelles. The division between prokaryotes and eukaryotes reflects the existence of two very different levels of cellular organization. Distinctive types of prokaryotes include extremophiles and methanogens; these are common in some extreme environments.[1]

Proteins

Proteins (/ˈproʊˌtiːnz/ or /ˈproʊti.ᵻnz/) are large biomolecules, or macromolecules, consisting of one or more long chains of amino acidresidues. Proteins perform a vast array of functions within living organisms, including catalyzing metabolic reactions, DNA replication,responding to stimuli, and transporting molecules from one location to another. Proteins differ from one another primarily in their sequence of […]

Proteins (/?pro??ti?nz/ or /?pro?ti.?nz/) are large biomolecules, or macromolecules, consisting of one or more long chains of amino acidresidues. Proteins perform a vast array of functions within living organisms, including catalyzing metabolic reactions, DNA replication,responding to stimuli, and transporting molecules from one location to another. Proteins differ from one another primarily in their sequence of amino acids, which is dictated by the nucleotide sequence of their genes, and which usually results in protein folding into a specific three-dimensional structure that determines its activity.

A linear chain of amino acid residues is called a polypeptide. A protein contains at least one long polypeptide. Short polypeptides, containing less than 20-30 residues, are rarely considered to be proteins and are commonly called peptides, or sometimes oligopeptides. The individual amino acid residues are bonded together by peptide bonds and adjacent amino acid residues. The sequence of amino acid residues in a protein is defined by the sequence of a gene, which is encoded in the genetic code. In general, the genetic code specifies 20 standard amino acids; however, in certain organisms the genetic code can include selenocysteine and—in certain archaeapyrrolysine. Shortly after or even during synthesis, the residues in a protein are often chemically modified by posttranslational modification, which alters the physical and chemical properties, folding, stability, activity, and ultimately, the function of the proteins. Sometimes proteins have non-peptide groups attached, which can be called prosthetic groups or cofactors. Proteins can also work together to achieve a particular function, and they often associate to form stable protein complexes.

Once formed, proteins only exist for a certain period of time and are then degraded and recycled by the cell’s machinery through the process of protein turnover. A protein’s lifespan is measured in terms of its half-life and covers a wide range. They can exist for minutes or years with an average lifespan of 1–2 days in mammalian cells. Abnormal and or misfolded proteins are degraded more rapidly either due to being targeted for destruction or due to being unstable.

Like other biological macromolecules such as polysaccharides and nucleic acids, proteins are essential parts of organisms and participate in virtually every process within cells. Many proteins are enzymes that catalyze biochemical reactions and are vital to metabolism. Proteins also have structural or mechanical functions, such as actin and myosin in muscle and the proteins in the cytoskeleton, which form a system of scaffolding that maintains cell shape. Other proteins are important incell signaling, immune responses, cell adhesion, and the cell cycle. Proteins are also necessary in animals’ diets, since animals cannot synthesize all the amino acids they need and must obtain essential amino acids from food. Through the process of digestion, animals break down ingested protein into free amino acids that are then used in metabolism.

Proteins may be purified from other cellular components using a variety of techniques such as ultracentrifugation, precipitation, electrophoresis, and chromatography; the advent of genetic engineering has made possible a number of methods to facilitate purification. Methods commonly used to study protein structure and function includeimmunohistochemistry, site-directed mutagenesis, X-ray crystallography, nuclear magnetic resonance and mass spectrometry.

In chemistry, hydrophobicity is the physical property of a molecule (known as a hydrophobe) that is seemingly repelled from a mass ofwater.[1] (Strictly speaking, there is no repulsive force involved; it is an absence of attraction.)

Hydrophobic molecules tend to be non-polar and, thus, prefer other neutral molecules and non-polar solvents. Hydrophobic molecules in water often cluster together, forming micelles. Water on hydrophobic surfaces will exhibit a high contact angle.

Examples of hydrophobic molecules include the alkanes, oils, fats, and greasy substances in general. Hydrophobic materials are used for oil removal from water, the management of oil spills, and chemical separation processes to remove non-polar substances from polar compounds.[2]

Hydrophobic is often used interchangeably with lipophilic, “fat-loving.” However, the two terms are not synonymous. While hydrophobic substances are usually lipophilic, there are exceptions—such as the silicones and fluorocarbons.

The term hydrophobe comes from the Ancient Greek ?????????, “having a horror of water”, constructed from ????, “water”, and ?????, “fear”.[3]

A hydrophilic molecule or portion of a molecule is one whose interactions with water and other polar substances are more thermodynamically favorable than their interactions with oil or other hydrophobic solvents.[2][3] They are typically charge-polarized and capable of hydrogen bonding. This makes these molecules soluble not only in water but also in other polar solvents.

Hydrophilic molecules (and portions of molecules) can be contrasted with hydrophobic molecules (and portions of molecules). In some cases, both hydrophilic and hydrophobic properties occur in a single molecule. An example of these amphiphilic molecules is the lipids that comprise the cell membrane. Another example is soap, which has a hydrophilic head and a hydrophobic tail, allowing it to dissolve in both water and oil.

Hydrophilic and hydrophobic molecules are also known as polar molecules and nonpolar molecules, respectively. Some hydrophilic substances do not dissolve. This type of mixture is called a colloid.

An approximate rule of thumb for hydrophilicity of organic compounds is that solubility of a molecule in water is more than 1 mass % if there is at least one neutral hydrophile group per 5 carbons, or at least one electrically charged hydrophile group per 7 carbons.[4]

Hydrophilic substances (ex: salts) can seem to attract water out of the air. Sugar is also hydrophilic, and like salt is sometimes used to draw water out of foods. Sugar sprinkled on cut fruit will “draw out the water” through hydrophilia, making the fruit mushy and wet, as in a common strawberry compote recipe.

trait theory

In psychology, trait theory (also called dispositional theory) is an approach to the study of human personality. Trait theorists are primarily interested in the measurement of traits, which can be defined as habitual patterns of behavior, thought, and emotion.[1]According to this perspective, traits are relatively stable over time, differ across individuals (e.g. some people are […]

In psychology, trait theory (also called dispositional theory) is an approach to the study of human personality. Trait theorists are primarily interested in the measurement of traits, which can be defined as habitual patterns of behavior, thought, and emotion.[1]According to this perspective, traits are relatively stable over time, differ across individuals (e.g. some people are outgoing whereas others are shy), and influence behavior. Traits are in contrast to states which are more transitory dispositions.

In some theories and systems, traits are something a person either has or does not have, but in many others traits are dimensions such as extraversion vs. introversion, with each person rating somewhere along this spectrum.

Gordon Allport was an early pioneer in the study of traits, which he also referred to as dispositions. In his approach, “cardinal” traits are those that dominate and shape a person’s behavior; their ruling passions/obsessions, such as a need for money, fame etc. By contrast, “central” traits such as honesty are characteristics found in some degree in every person – and finally “secondary” traits are those seen only in certain circumstances (such as particular likes or dislikes that a very close friend may know), which are included to provide a complete picture of human complexity.

A wide variety of alternative theories and scales were later developed, including:

Currently, two general approaches are the most popular:

Neuroticism is a fundamental personality trait in the study of psychology characterized by anxiety, fear, moodiness, worry, envy, frustration, jealousy, and loneliness.[1] Individuals who score high on neuroticism are more likely than the average to experience such feelings as anxiety, anger, envy, guilt, and depressed mood.[2] They respond more poorly tostressors, are more likely to interpret ordinary situations as threatening, and minor frustrations as hopelessly difficult. They are often self-conscious and shy, and they may have trouble controlling urges and delaying gratification. Neuroticism is a prospective risk factor for most “common mental disorders“,[3] such as depression, phobia, panic disorder, other anxiety disorders, and substance use disorder—symptoms that traditionally have been called neuroses.[3][4][5][6][7]

Neuroticism appears to be related to physiological differences in the brain. Hans Eysenck theorized that neuroticism is a function of activity in the limbic system, and his research suggests that people who score highly on measures of neuroticism have a more reactive sympathetic nervous system, and are more sensitive to environmental stimulation.[20]

Behavioral genetics researchers have found that a significant portion of the variability on measures of neuroticism can be attributed to genetic factors.[21]

A study with positron emission tomography has found that healthy subjects that score high on the NEO PI-R neuroticism dimension tend to have high altanserin binding in the frontolimbic region of the brain—an indication that these subjects tend to have more of the 5-HT2A receptor in that location.[22] Another study has found that healthy subjects with a high neuroticism score tend to have higher DASB binding in the thalamus; DASB is a ligand that binds to the serotonin transporter protein.[23]

Another neuroimaging study using magnetic resonance imaging to measure brain volume found that the brain volume was negatively correlated to NEO PI-R neuroticism when correcting for possible effects of intracranial volume, sex, and age.[24]

The results of one study found that, on average, women score moderately higher than men on neuroticism. This study examined sex differences in the ‘Big Five’ personality traits across 55 nations. It found that across the 55 nations studied, the most pronounced difference was in neuroticism.[33] This study found that in 49 of the 55 nations studied, women scored higher in neuroticism than men. In no country did men report significantly higher neuroticism than women.

Neuroticism, along with other personality traits, has been mapped across states in the USA. People in eastern states such as New York, New Jersey, West Virginia, and Mississippi tend to score high on neuroticism, whereas people in many western states, such as Utah, Colorado, South Dakota, Oregon, and Arizona score lower on average. People in states that are higher in neuroticism also tend to have higher rates of heart disease and lower life expectancy.[34]

One of the theories regarding evolutionary approaches to depression focuses on neuroticism. A moderate amount of neuroticism may provide benefits, such as increased drive and productivity, due to greater sensitivity to negative outcomes. Too much, however, may reduce fitness by producing, for example, recurring depressions. Thus, evolution will select for an optimal amount and most people will have neuroticism near this optimum. However, because neuroticism likely has a normal distribution in the population, a minority will be highly neurotic.[35]

VIA Inventory of Strengths (VIA-IS)

Classification of strengths Wisdom and Knowledge: creativity, curiosity, judgment, love of learning, perspective Courage: bravery, perseverance, honesty, zest Humanity: love, kindness, social intelligence Justice: teamwork, fairness, leadership Temperance: forgiveness, humility, prudence, self-regulation Transcendence: appreciation of beauty and excellence, gratitude, hope, humor, spirituality[3] The VIA Inventory of Strengths (VIA-IS), formerly known as the “Values in Action […]

Classification of strengths

  1. Wisdom and Knowledge: creativity, curiosity, judgment, love of learning, perspective
  2. Courage: bravery, perseverance, honesty, zest
  3. Humanity: love, kindness, social intelligence
  4. Justice: teamwork, fairness, leadership
  5. Temperance: forgiveness, humility, prudence, self-regulation
  6. Transcendence: appreciation of beauty and excellence, gratitude, hope, humor, spirituality[3]

The VIA Inventory of Strengths (VIA-IS), formerly known as the “Values in Action Inventory,” is a psychological assessment measure designed to identify an individual’s profile of character strengths. It was created by Christopher Peterson and Martin Seligman, well-known researchers in the field of positive psychology, in order to operationalize theirCharacter Strengths and Virtues Handbook (CSV).[1] The CSV is the positive psychology counterpart to the Diagnostic and Statistical Manual of Mental Disorders (DSM) used in traditional psychology.[1] Unlike the DSM, which scientifically categorizes human deficits and disorders, the CSV classifies positive human strengths.[2] Moreover, the CSV is centered on helping people recognize and build upon their strengths. This aligned with the overall goal of the positive psychology movement, which aims to make people’s lives more fulfilling, rather than simply treating mental illness.[2] Notably, the VIA-IS is the tool by which people can identify their own positive strengths and learn how to capitalize on them.[2]

As a relatively new field of research, positive psychology lacked a common vocabulary for discussing measurable positive traits before 2004.[1] Traditional psychology benefited from the creation of DSM, as it provided researchers and clinicians with the same set of language from which they could talk about the negative. As a first step in remedying this disparity between tradition and positive psychology, Peterson and Seligman set out to identify, organize and measure character.

Peterson & Seligman began by defining the notion of character as traits that are possessed by an individual and are stable over time, but can still be impacted by setting and thus are subject to change.[1] The researchers then started the process of identifying character strengths and virtues by brainstorming with a group of noted positive psychology scholars. Then, Peterson & Seligman examined ancient cultures (including their religions, politics, education and philosophies) for information about how people in the past construed human virtue. The researchers looked for virtues that were present across cultures and time. Six core virtues emerged from their analysis: courage, justice, humanity, temperance, transcendence and wisdom.

Next, Peterson and Seligman proposed a model of classification which includes horizontal and vertical components. The hierarchical system is modeled after the Linnaean classification of species, which ranges from a specific species to more general and broad categories. The scientists stated the six core values are the broadest category and are, “core characteristics valued by moral philosophers and religious thinkers” (p. 13).[1] Peterson and Seligman then moved down the hierarchy to identifying character strengths, which are, “the psychological processes or mechanisms that define the virtues” (p. 13).[1]

The researchers began the process of identifying individual character strengths by brainstorming with a group of noted positive psychology scholars.[1] This exercise generated a list of human strengths, which were helpful when consulting with Gallup Organization. Peterson and Seligman then performed an exhaustive literature search for work that directly addresses good character in the domains of, “psychiatry, youth development, philosophy and psychology” (p. 15). Some individuals who influenced Peterson and Seligman’s choice of strengths include: Abraham Maslow, Erik Erikson, Ellen Greenberger, Marie Jahoda, Carol Ryff, Michael Cawley, Howard Gardner, Shalom Schwartz. In an effort to leave no stone unturned, the researchers also looked for virtue-laden messages in popular culture. For example, the researchers examined Hallmark greeting cards, personal ads, graffiti, bumper stickers and profiles of Pokémon characters.

After identifying dozens of ‘candidate strengths’, the researchers needed to find a way to further refine their list. Therefore, Peterson & Seligman developed a list of 10 criteria (e.g., strengths must contribute to a sense of a fulfilling life, must be intrinsically valuable) to help them select the final 24 strengths for the CSV (see CSV for complete list of criteria). Approximately half of the strengths included in the CSV meet all 10 criteria, and half do not.[1] By looking for similarities between candidate strengths, the researchers distributed 24 character strengths between six virtue categories. Only after creating this a priori organization of traits, the researchers performed, “an exploratory factor analysis of scale scores using varimax rotation,” (p. 632) from which five factors emerged.[1] Peterson & Seligman state that they are not as concerned with how the 24 strengths are grouped into virtue clusters because, in the end, these traits are mixed together to form the character of a person.

Only 3 studies have checked the factor structure of the CSV, on which the VIA-IS is based.[1][9][10]

Using a second order factor analysis, Macdonald & colleagues (2008) found that the 24 strengths did not fit into the 6 higher order virtues model proposed in the CSV. None of the clusters of characters strengths that they found resembled the structure of the 6 virtue clusters of strengths. The researchers noted that many of the VIA character strengths cross-loaded onto multiple factors. Rather, the strengths were best represented by a one and four factor model. A one factor model would mean that the strengths are best accounted for by, “one overarching factor,” such as a global trait of character (p. 797).[9] A four factor model more closely resembles the ‘Big Five’ model of personality. The character strengths in the four factor model could be organized into the following four groups: Niceness, Positivity, Intellect and Conscientiousness.

Peterson and Seligman (2004) conducted a factor analysis and found that a five factor model, rather than their 6 hierarchical virtues model, best organized the strengths. Their study, however, did not include five of the character strengths in the results of their analysis. The researchers most likely did this because their results were plagued by the problem of strengths cross-loading on to multiple factors, similar to what occurred in Macdonald and colleagues (2008) study.[10] Clearly, empirical evidence casts doubt on the link proposed by Peterson & Seligman (2004) between the 24 strengths and associated 6 higher order virtues.

Brdar & Kashdan (2009) used more precise statistical tools to build upon the findings of the two earlier studies. They found that a four factor model (Interpersonal Strengths, Vitality, Fortitude and Cautiousness) explained 60% of the variance. One large, overarching factor explained 50% of the variance. The four factors found by Brdar and Kashdan (2009) are similar to the four factors found by Macdonald and colleagues (2008). Once again, the Brdar and Kashdan found that the 24 strengths did not fall into the 6 higher order virtues proposed by Peterson and Seligman (2004). The correlations found between many of the strengths demonstrates that each strength is not distinct, which contradicts the claims made by the creators of the VIA-IS.

Caution should be taken in interpreting the results from these three studies as their samples differ in age and country of origin.[10]

Caso Philip Morris contra Uruguay

The Philip Morris v. Uruguay case (Spanish: Caso Philip Morris contra Uruguay) started on 19 February 2010, when the multinational tobacco company Philip Morris International filed a complaint against Uruguay.[1] The company complains that Uruguay’s anti-smoking legislation devalues its cigarette … Continue reading

The Philip Morris v. Uruguay case (Spanish: Caso Philip Morris contra Uruguay) started on 19 February 2010, when the multinational tobacco company Philip Morris International filed a complaint against Uruguay.[1] The company complains that Uruguay’s anti-smoking legislation devalues its cigarette trademarks and investments in the country and is suing Uruguay for compensation under the bilateral investment treaty between Switzerland and Uruguay.[2] (Philip Morris is headquartered inLausanne.)[3] The treaty provides that disputes are settled by binding arbitration before the International Centre for Settlement of Investment Disputes (ICSID).

Uruguay had received accolades from the World Health Organization and from anti-smoking activists for its anti-smoking campaign.[4]

The is-ought problem

The is-ought problem, as articulated by Scottish philosopher and historian David Hume (1711–76), states that many writers make claims about what ought to be on the basis of statements about what is. Hume found that there seems to be a … Continue reading

The is-ought problem, as articulated by Scottish philosopher and historian David Hume (1711–76), states that many writers make claims about what ought to be on the basis of statements about what is. Hume found that there seems to be a significant difference betweenpositive statements (about what is) and prescriptive or normative statements (about what ought to be), and that it is not obvious how one can coherently move from descriptive statements to prescriptive ones. The is–ought problem is also known as Hume’s law, or Hume’s guillotine.

A similar view is defended by G. E. Moore‘s open-question argument, intended to refute any identification of moral properties with naturalproperties. This so-called naturalistic fallacy stands in contrast to the views of ethical naturalists.