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Glucocorticoid

Glucocorticoids (or, less commonly, glucocorticosteroids) are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor that is present in almost every vertebrate animal cell. The name "glucocorticoid" is a portmanteau (glucose + cortex + steroid) and is composed from its role in regulation of glucose metabolism, synthesis in the adrenal cortex, and its steroidal structure (see structure below).

Glucocorticoids are part of the feedback mechanism in the immune system, which reduces certain aspects of immune function, such as inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. Glucocorticoids have many diverse effects such as pleiotropy, including potentially harmful side effects. They also interfere with some of the abnormal mechanisms in cancer cells, so they are used in high doses to treat cancer. This includes inhibitory effects on lymphocyte proliferation, as in the treatment of lymphomas and leukemias, and the mitigation of side effects of anticancer drugs.

Glucocorticoids affect cells by binding to the glucocorticoid receptor. The activated glucocorticoid receptor-glucocorticoid complex up-regulates the expression of anti-inflammatory proteins in the nucleus (a process known as transactivation) and represses the expression of pro-inflammatory proteins in the cytosol by preventing the translocation of other transcription factors from the cytosol into the nucleus (transrepression).

Glucocorticoids are distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects. In technical terms, "corticosteroid" refers to both glucocorticoids and mineralocorticoids (as both are mimics of hormones produced by the adrenal cortex), but is often used as a synonym for "glucocorticoid". Glucocorticoids are chiefly produced in the zona fasciculata of the adrenal cortex, whereas mineralocorticoids are synthesized in the zona glomerulosa.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life, and it regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions. Increases in glucocorticoid concentrations are an integral part of stress response and are the most commonly used biomarkers to measure stress. Glucocorticoids have numerous non-stress-related functions as well, and glucocorticoid concentrations can increase in response to pleasure or excitement. Various synthetic glucocorticoids are available; these are widely utilized in general medical practice and numerous specialties, either as replacement therapy in glucocorticoid deficiency or to suppress the body's immune system.

Effects

Glucocorticoid effects may be broadly classified into two major categories: immunological and metabolic. In addition, glucocorticoids play important roles in fetal development and body fluid homeostasis.

Immune
Glucocorticoids function via interaction with the glucocorticoid receptor (see details below):
 * Upregulate the expression of anti-inflammatory proteins.
 * Downregulate the expression of proinflammatory proteins.

Glucocorticoids are also shown to play a role in the development and homeostasis of T lymphocytes. This has been shown in transgenic mice with either increased or decreased sensitivity of T cell lineage to glucocorticoids.

Metabolic
The name "glucocorticoid" derives from early observations that these hormones were involved in glucose metabolism. In the fasted state, cortisol stimulates several processes that collectively serve to increase and maintain normal concentrations of glucose in the blood.

Metabolic effects:
 * Stimulation of gluconeogenesis, in particular, in the liver: This pathway results in the synthesis of glucose from non-hexose substrates, such as amino acids and glycerol from triglyceride breakdown, and is particularly important in carnivores and certain herbivores. Enhancing the expression of enzymes involved in gluconeogenesis is probably the best-known metabolic function of glucocorticoids.
 * Mobilization of amino acids from extrahepatic tissues: These serve as substrates for gluconeogenesis.
 * Inhibition of glucose uptake in muscle and adipose tissue: A mechanism to conserve glucose
 * Stimulation of fat breakdown in adipose tissue: The fatty acids released by lipolysis are used for production of energy in tissues like muscle, and the released glycerol provide another substrate for gluconeogenesis.
 * Increase in sodium retention and potassium excretion leads to hypernatremia and hypokalemia
 * Increase in hemoglobin concentration, likely due to hindrance of the ingestion of red blood cell by macrophage or other phagocyte.
 * Increased urinary uric acid
 * Increased urinary calcium and hypocalcemia
 * Alkalosis
 * Leukocytosis

Excessive glucocorticoid levels resulting from administration as a drug or hyperadrenocorticism have effects on many systems. Some examples include inhibition of bone formation, suppression of calcium absorption (both of which can lead to osteoporosis), delayed wound healing, muscle weakness, and increased risk of infection. These observations suggest a multitude of less-dramatic physiologic roles for glucocorticoids.

Developmental
Glucocorticoids have multiple effects on fetal development. An important example is their role in promoting maturation of the lung and production of the surfactant necessary for extrauterine lung function. Mice with homozygous disruptions in the corticotropin-releasing hormone gene (see below) die at birth due to pulmonary immaturity. In addition, glucocorticoids are necessary for normal brain development, by initiating terminal maturation, remodeling axons and dendrites, and affecting cell survival and may also play a role in hippocampal development. Glucocorticoids stimulate the maturation of the Na+/K+/ATPase, nutrient transporters, and digestion enzymes, promoting the development of a functioning gastro-intestinal system. Glucocorticoids also support the development of the neonate's renal system by increasing glomerular filtration.

Arousal and cognition

Glucocorticoids act on the hippocampus, amygdala, and frontal lobes. Along with adrenaline, these enhance the formation of flashbulb memories of events associated with strong emotions, both positive and negative. This has been confirmed in studies, whereby blockade of either glucocorticoids or noradrenaline activity impaired the recall of emotionally relevant information. Additional sources have shown subjects whose fear learning was accompanied by high cortisol levels had better consolidation of this memory (this effect was more important in men). The effect that glucocorticoids have on memory may be due to damage specifically to the CA1 area of the hippocampal formation.

In multiple animal studies, prolonged stress (causing prolonged increases in glucocorticoid levels) have shown destruction of the neurons in the hippocampus area of the brain, which has been connected to lower memory performance.

Glucocorticoids have also been shown to have a significant impact on vigilance (attention deficit disorder) and cognition (memory). This appears to follow the Yerkes-Dodson curve, as studies have shown circulating levels of glucocorticoids vs. memory performance follow an upside-down U pattern, much like the Yerkes-Dodson curve. For example, long-term potentiation (LTP; the process of forming long-term memories) is optimal when glucocorticoid levels are mildly elevated, whereas significant decreases of LTP are observed after adrenalectomy (low-glucocorticoid state) or after exogenous glucocorticoid administration (high-glucocorticoid state). Elevated levels of glucocorticoids enhance memory for emotionally arousing events, but lead more often than not to poor memory for material unrelated to the source of stress/emotional arousal. In contrast to the dose-dependent enhancing effects of glucocorticoids on memory consolidation, these stress hormones have been shown to inhibit the retrieval of already stored information. Long-term exposure to glucocorticoid medications, such as asthma and anti-inflammatory medication, has been shown to create deficits in memory and attention both during and, to a lesser extent, after treatment, a condition known as "steroid dementia".

Body fluid homeostasis
Glucocorticoids could act centrally, as well as peripherally, to assist in the normalization of extracellular fluid volume by regulating body's action to atrial natriuretic peptide (ANP). Centrally, glucocorticoids could inhibit dehydration-induced water intake; peripherally, glucocorticoids could induce a potent diuresis.

Transactivation
Glucocorticoids bind to the cytosolic glucocorticoid receptor, a type of nuclear receptor that is activated by ligand binding. After a hormone binds to the corresponding receptor, the newly formed complex translocates itself into the cell nucleus, where it binds to glucocorticoid response elements in the promoter region of the target genes resulting in the regulation of gene expression. This process is commonly referred to as transcriptional activation, or transactivation.

The proteins encoded by these up-regulated genes have a wide range of effects, including, for example:
 * Anti-inflammatory – lipocortin I, p11/calpactin binding protein, secretory leukocyte protease inhibitor 1 (SLPI), and Mitogen-activated protein kinase phosphatase (MAPK phosphatase)
 * Increased gluconeogenesis – glucose 6-phosphatase and tyrosine aminotransferase

Transrepression
The opposite mechanism is called transcriptional repression, or transrepression. The classical understanding of this mechanism is that activated glucocorticoid receptor binds to DNA in the same site where another transcription factor would bind, which prevents the transcription of genes that are transcribed via the activity of that factor. While this does occur, the results are not consistent for all cell types and conditions; there is no generally accepted, general mechanism for transrepression.

New mechanisms are being discovered where transcription is repressed, but the activated glucocorticoid receptor is not interacting with DNA, but rather with another transcription factor directly, thus interfering with it, or with other proteins that interfere with the function of other transcription factors. This latter mechanism appears to be the most likely way that activated glucocorticoid receptor interferes with NF-κB - namely by recruiting histone deacetylase, which deacetylate the DNA in the promoter region leading to closing of the chromatin structure where NF-κB needs to bind.

Nongenomic effects
Activated glucocorticoid receptor has effects that have been experimentally shown to be independent of any effects on transcription and can only be due to direct binding of activated glucocorticoid receptor with other proteins or with mRNA.

For example, Src kinase which binds to inactive glucocorticoid receptor, is released when a glucocorticoid binds to glucocorticoid receptor, and phosphorylates a protein that in turn displaces an adaptor protein from a receptor important in inflammation, epidermal growth factor, reducing its activity, which in turn results in reduced creation of arachidonic acid – a key proinflammatory molecule. This is one mechanism by which glucocorticoids have an anti-inflammatory effect.

Pharmacology

A variety of synthetic glucocorticoids, some far more potent than cortisol, have been created for therapeutic use. They differ in both pharmacokinetics (absorption factor, half-life, volume of distribution, clearance) and pharmacodynamics (for example the capacity of mineralocorticoid activity: retention of sodium (Na$+$) and water; renal physiology). Because they permeate the intestines easily, they are administered primarily per os (by mouth), but also by other methods, such as topically on skin. More than 90% of them bind different plasma proteins, though with a different binding specificity. Endogenous glucocorticoids and some synthetic corticoids have high affinity to the protein transcortin (also called corticosteroid-binding globulin), whereas all of them bind albumin. In the liver, they quickly metabolize by conjugation with a sulfate or glucuronic acid, and are secreted in the urine.

Glucocorticoid potency, duration of effect, and the overlapping mineralocorticoid potency vary. Cortisol is the standard of comparison for glucocorticoid potency. Hydrocortisone is the name used for pharmaceutical preparations of cortisol.

The data below refer to oral administration. Oral potency may be less than parenteral potency because significant amounts (up to 50% in some cases) may not reach the circulation. Fludrocortisone acetate and deoxycorticosterone acetate are, by definition, mineralocorticoids rather than glucocorticoids, but they do have minor glucocorticoid potency and are included in this table to provide perspective on mineralocorticoid potency.

Therapeutic use
Glucocorticoids may be used in low doses in adrenal insufficiency. In much higher doses, oral or inhaled glucocorticoids are used to suppress various allergic, inflammatory, and autoimmune disorders. Inhaled glucocorticoids are the second-line treatment for asthma. They are also administered as post-transplantory immunosuppressants to prevent the acute transplant rejection and the graft-versus-host disease. Nevertheless, they do not prevent an infection and also inhibit later reparative processes. Newly emerging evidence showed that glucocorticoids could be used in the treatment of heart failure to increase the renal responsiveness to diuretics and natriuretic peptides. Glucocorticoids are historically used for pain relief in inflammatory conditions. However, corticosteroids show limited efficacy in pain relief and potential adverse events for their use in tendinopathies.

Replacement
Any glucocorticoid can be given in a dose that provides approximately the same glucocorticoid effects as normal cortisol production; this is referred to as physiologic, replacement, or maintenance dosing. This is approximately 6–12 mg/m2/day of hydrocortisone (m2 refers to body surface area (BSA), and is a measure of body size; an average man's BSA is 1.9 m2).

Therapeutic immunosuppression
Glucocorticoids cause immunosuppression, and the therapeutic component of this effect is mainly the decreases in the function and numbers of lymphocytes, including both B cells and T cells.

The major mechanism for this immunosuppression is through inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). NF-κB is a critical transcription factor involved in the synthesis of many mediators (i.e., cytokines) and proteins (i.e., adhesion proteins) that promote the immune response. Inhibition of this transcription factor, therefore, blunts the capacity of the immune system to mount a response.

Glucocorticoids suppress cell-mediated immunity by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and IFN-γ, the most important of which is IL-2. Smaller cytokine production reduces the T cell proliferation.

Glucocorticoids, however, not only reduce T cell proliferation, but also lead to another well known effect - glucocorticoid-induced apoptosis. The effect is more prominent in immature T cells still inside in the thymus, but peripheral T cells are also affected. The exact mechanism regulating this glucocorticoid sensitivity lies in the Bcl-2 gene.

Glucocorticoids also suppress the humoral immunity, thereby causing a humoral immune deficiency. Glucocorticoids cause B cells to express smaller amounts of IL-2 and of IL-2 receptors. This diminishes both B cell clone expansion and antibody synthesis. The diminished amounts of IL-2 also cause fewer T lymphocyte cells to be activated.

The effect of glucocorticoids on Fc receptor expression in immune cells is complicated. Dexamethasone decreases IFN-gamma stimulated Fc gamma RI expression in neutrophils while conversely causing an increase in monocytes. Glucocorticoids may also decrease the expression of Fc receptors in macrophages, but the evidence supporting this regulation in earlier studies has been questioned. The effect of Fc receptor expression in macrophages is important since it is necessary for the phagocytosis of opsonised cells. This is because Fc receptors bind antibodies attached to cells targeted for destruction by macrophages.

Anti-inflammatory
Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2, thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events (epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes. They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase/PGE isomerase (COX-1 and COX-2), the latter effect being much like that of NSAIDs, thus potentiating the anti-inflammatory effect.

In addition, glucocorticoids also suppress cyclooxygenase expression.

Glucocorticoids marketed as anti-inflammatories are often topical formulations, such as nasal sprays for rhinitis or inhalers for asthma. These preparations have the advantage of only affecting the targeted area, thereby reducing side effects or potential interactions. In this case, the main compounds used are beclometasone, budesonide, fluticasone, mometasone and ciclesonide. In rhinitis, sprays are used. For asthma, glucocorticoids are administered as inhalants with a metered-dose or dry powder inhaler. In rare cases, symptoms of radiation induced thyroiditis has been treated with oral glucocorticoids.

Hyperaldosteronism
Glucocorticoids can be used in the management of familial hyperaldosteronism type 1. They are not effective, however, for use in the type 2 condition.

Heart failure
Glucocorticoids could be used in the treatment of decompensated heart failure to potentiate renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large doses of loop diuretics.

Resistance

Resistance to the therapeutic uses of glucocorticoids can present difficulty; for instance, 25% of cases of severe asthma may be unresponsive to steroids. This may be the result of genetic predisposition, ongoing exposure to the cause of the inflammation (such as allergens), immunological phenomena that bypass glucocorticoids, pharmacokinetic disturbances (incomplete absorption or accelerated excretion or metabolism) and viral and/or bacterial respiratory infections.

Side effects
Glucocorticoid drugs currently being used act nonselectively, so in the long run they may impair many healthy anabolic processes. To prevent this, much research has been focused recently on the elaboration of selectively acting glucocorticoid drugs. Side effects include:
 * Immunodeficiency (see section below)
 * Hyperglycemia due to increased gluconeogenesis, insulin resistance, and impaired glucose tolerance ("steroid diabetes"); caution in those with diabetes mellitus
 * Increased skin fragility, easy bruising
 * Negative calcium balance due to reduced intestinal calcium absorption
 * Steroid-induced osteoporosis: reduced bone density (osteoporosis, osteonecrosis, higher fracture risk, slower fracture repair)
 * Weight gain due to increased visceral and truncal fat deposition (central obesity) and appetite stimulation; see corticosteroid-induced lipodystrophy
 * Hypercortisolemia with prolonged or excessive use (also known as, exogenous Cushing's syndrome)
 * Impaired memory and attention deficits See steroid dementia syndrome.
 * Adrenal insufficiency (if used for long time and stopped suddenly without a taper)
 * Muscle and tendon breakdown (proteolysis), weakness, reduced muscle mass and repair
 * Expansion of malar fat pads and dilation of small blood vessels in skin
 * Lipomatosis within the epidural space
 * Excitatory effect on central nervous system (euphoria, psychosis)
 * Anovulation, irregularity of menstrual periods
 * Growth failure, delayed puberty
 * Increased plasma amino acids, increased urea formation, negative nitrogen balance
 * Glaucoma due to increased ocular pressure
 * Cataracts
 * Topical steroid withdrawal

In high doses, hydrocortisone (cortisol) and those glucocorticoids with appreciable mineralocorticoid potency can exert a mineralocorticoid effect as well, although in physiologic doses this is prevented by rapid degradation of cortisol by 11β-hydroxysteroid dehydrogenase isoenzyme 2 (11β-HSD2) in mineralocorticoid target tissues. Mineralocorticoid effects can include salt and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis.

Immunodeficiency
Glucocorticoids cause immunosuppression, decreasing the function and/or numbers of neutrophils, lymphocytes (including both B cells and T cells), monocytes, macrophages, and the anatomical barrier function of the skin. This suppression, if large enough, can cause manifestations of immunodeficiency, including T cell deficiency, humoral immune deficiency and neutropenia.

Withdrawal
In addition to the effects listed above, use of high-dose glucocorticoids for only a few days begins to produce suppression of the patient's adrenal glands suppressing hypothalamic corticotropin-releasing hormone (CRH) leading to suppressed production of adrenocorticotropic hormone (ACTH) by the anterior pituitary. With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid.

During this recovery time, the patient is vulnerable to adrenal insufficiency during times of stress, such as illness. While suppressive dose and time for adrenal recovery vary widely, clinical guidelines have been devised to estimate potential adrenal suppression and recovery, to reduce risk to the patient. The following is one example:
 * If patients have been receiving daily high doses for five days or less, they can be abruptly stopped (or reduced to physiologic replacement if patients are adrenal-deficient). Full adrenal recovery can be assumed to occur by a week afterward.
 * If high doses were used for six to 10 days, reduce to replacement dose immediately and taper over four more days. Adrenal recovery can be assumed to occur within two to four weeks of completion of steroids.
 * If high doses were used for 11–30 days, cut immediately to twice replacement, and then by 25% every four days. Stop entirely when dose is less than half of replacement. Full adrenal recovery should occur within one to three months of completion of withdrawal.
 * If high doses were used more than 30 days, cut dose immediately to twice replacement, and reduce by 25% each week until replacement is reached. Then change to oral hydrocortisone or cortisone as a single morning dose, and gradually decrease by 2.5 mg each week. When the morning dose is less than replacement, the return of normal basal adrenal function may be documented by checking 0800 cortisol levels prior to the morning dose; stop drugs when 0800 cortisol is 10 μg/dl. Predicting the time to full adrenal recovery after prolonged suppressive exogenous steroids is difficult; some people may take nearly a year.
 * Flare-up of the underlying condition for which steroids are given may require a more gradual taper than outlined above.

title: Glucocorticoid


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Personal construct theory

Within personality psychology, personal construct theory (PCT) or personal construct psychology (PCP) is a theory of personality and cognition developed by the American psychologist George Kelly in the 1950s. The theory addresses the psychological reasons for actions. Kelly proposed that individuals can be psychologically evaluated according to similarity–dissimilarity poles, which he called personal constructs (schemas, or ways of seeing the world). The theory is considered by some psychologists as forerunner to theories of cognitive therapy.

From the theory, Kelly derived a psychotherapy approach, as well as a technique called the repertory grid interview, that helped his patients to analyze their own personal constructs with minimal intervention or interpretation by the therapist. The repertory grid was later adapted for various uses within organizations, including decision-making and interpretation of other people's world-views. The UK Council for Psychotherapy, a regulatory body, classifies PCP therapy within the experiential subset of the constructivist school.

Principles
A main tenet of PCP theory is that a person's unique psychological processes are channeled by the way they anticipate events. Kelly believed that anticipation and prediction are the main drivers of our mind. "Every man is, in his own particular way, a scientist", said Kelly: people are constantly building up and refining theories and models about how the world works so that they can anticipate future events. People start doing this at birth (for example, a child discovers that if they start to cry, their mother will come to them) and continue refining their theories as they grow up.

Kelly proposed that every construct is bipolar, specifying how two things are similar to each other (lying on the same pole) and different from a third thing, and they can be expanded with new ideas. (More recent researchers have suggested that constructs need not be bipolar. ) People build theories—often stereotypes—about other people and also try to control them or impose on others their own theories so as to be better able to predict others' actions. All these theories are built up from a system of constructs. A construct has two extreme points, such as "happy–sad," and people tend to place items at either extreme or at some point in between. People's minds, said Kelly, are filled up with these constructs at a low level of awareness.

A given person, set of persons, any event, or circumstance can be characterized fairly precisely by the set of constructs applied to it and by the position of the thing within the range of each construct. For example, Fred may feel as though he is not happy or sad (an example of a construct); he feels as though he is between the two. However, he feels he is more clever than he is stupid (another example of a construct). A baby may have a preverbal construct of what behaviors may cause their mother to come to them. Constructs can be applied to anything people put their attention to, and constructs also strongly influence what people fix their attention on. People can construe reality by constructing different constructs. Hence, determining a person's system of constructs would go a long way towards understanding them, especially the person's essential constructs that represent their very strong and unchangeable beliefs and their self-construal.

Kelly did not use the concept of the unconscious; instead, he proposed the notion of "levels of awareness" to explain why people did what they did. He identified "construing" as the highest level and "preverbal" as the lowest level of awareness.

Some psychologists have suggested that PCT is not a psychological theory but a metatheory because it is a theory about theories.

Therapy approach
Kelly believed in a non-invasive or non-directive approach to psychotherapy. Rather than having the therapist interpret the person's psyche, which would amount to imposing the doctor's constructs on the patient, the therapist should just act as a facilitator of the patient finding his or her own constructs. The patient's behavior is then mainly explained as ways to selectively observe the world, act upon it and update the construct system in such a way as to increase predictability. To help the patient find his or her constructs, Kelly developed the repertory grid interview technique.

Kelly explicitly stated that each individual's task in understanding their personal psychology is to put in order the facts of his or her own experience. Then the individual, like the scientist, is to test the accuracy of that constructed knowledge by performing those actions the constructs suggest. If the results of their actions are in line with what the knowledge predicted, then they have done a good job of finding the order in their personal experience. If not, then they can modify the construct: their interpretations or their predictions or both. This method of discovering and correcting constructs is roughly analogous to the general scientific method that is applied in various ways by modern sciences to discover truths about the universe.

The repertory grid
The repertory grid serves as part of various assessment methods to elicit and examine an individual's repertoire of personal constructs. There are different formats such as card sorts, verbally administered group format, and the repertory grid technique.

The repertory grid itself is a matrix where the rows represent constructs found, the columns represent the elements, and cells indicate with a number the position of each element within each construct. There is software available to produce several reports and graphs from these grids.

To build a repertory grid for a patient, Kelly might first ask the patient to select about seven elements (although there are no fixed rules for the number of elements) whose nature might depend on whatever the patient or therapist are trying to discover. For instance, "Two specific friends, two work-mates, two people you dislike, your mother and yourself", or something of that sort. Then, three of the elements would be selected at random, and then the therapist would ask: "In relation to ... (whatever is of interest), in which way are two of these people alike but different from the third?" The answer is sure to indicate one of the extreme points of one of the patient's constructs. He might say for instance that Fred and Sarah are very communicative whereas John isn't. Further questioning would reveal the other end of the construct (say, introvert) and the positions of the three characters between extremes. Repeating the procedure with different sets of three elements ends up revealing several constructs the patient might not have been fully aware of.

In the book Personal Construct Methodology, researchers Brian R. Gaines and Mildred L.G. Shaw noted that they "have also found concept mapping and semantic network tools to be complementary to repertory grid tools and generally use both in most studies" but that they "see less use of network representations in PCP studies than is appropriate". They encouraged practitioners to use semantic network techniques in addition to the repertory grid.

Organizational applications
PCP has always been a minority interest among psychologists. During the last 30 years, it has gradually gained adherents in the US, Canada, the UK, Germany, Australia, Ireland, Italy and Spain. While its chief fields of application remain clinical and educational psychology, there is an increasing interest in its applications to organizational development, employee training and development, job analysis, job description and evaluation. The repertory grid is often used in the qualitative phase of market research, to identify the ways in which consumers construe products and services.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Personal construct theory


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Talk:Gwanggaeto the Great

Disputed history
CHINESE GOVERNMENT SHOULD ACCEPT " KORGURYO KINGDOM" AS KOREAN TERRITORY. YOU CANNOT CHANGE HISTORY. HISTORY IS TO LEARN FROM THE PAST, PRESENT, AND FOR THE FUTURE. WHAT CHINESE GOVERNMENT DOING WITH " NORTHEAST PROJECT" IS VERY VERY STUPID. TRUTH WILL ALWAYS PREVAIL. IT CAN ONLY CREATE FRICTION BETWEEN KOREANS AND CHINESE. IN THE END CHINESE WILL LOSE. LIKE TIBET, TAIWAN, CHINA ( WEST COAST PROVINCE) UIGHUR PROVINCE, AND MANCHURIA ( KOREA). THE WORD CHINA OR CHINA LAND IS VERY SUPERFICIAL LAND ONLY WAY CHINESE GOVERNMENT TO KEEP CONTROL 1.2 BILLION PEOPLE BY HAVING " COMMUNIST REGIME". EVEN COMMUNIST REGIME DON'T TELL THE TRUTH ABOUT CHINESE HISTORY. CHINESE GOVERNMENT IS KILLING THEMSELVES MAKING THEMSELVES LOOK VERY VERY STUPID. IN THE END KOREANS WILL WIN. —Preceding unsigned comment added by Population6 (talk • contribs) 01:50, 6 August 2008 (UTC)

The Chinese government maintains that Koguryŏ was a local Kingdom of a Chinese national minority, i.e. on Chinese territory. Please also refer to the discussion page on Koguryŏ. Babelfisch 07:52, 22 August 2005 (UTC)

so what? chinese can claim whatever they want...it won't change the history though Koguryo was never a chinese kingdom. chinese (mandarin) can only claim 'Han' dynasties as their historic kingdoms just because they forcefully dominate manchuria, tibet and east turkestan that doesn't mean they belonged to them 139.80.123.40 13:50, 30 April 2006 (UTC)

er...
some of this seems like someone began to rant about Korean history...especially that huge chunk without references.

--Heero Kirashami (talk) 19:50, 8 August 2009 (UTC)

Ainu?
There is no citation for Gwanggaeto attacking Ainu peoples. Is it implying there were Ainu settlements in Manchuria/Southern Siberia? — Preceding unsigned comment added by Rekishiotaku (talk • contribs) 12:24, 4 July 2011 (UTC)

The great?
The title, Gwanggaeto the great has to be changed into Emperor Gwanggaeto since the rulers of Goguryeo were called "Taewang" from the reign of Micheon. — Preceding unsigned comment added by 222.101.9.93 (talk) 09:52, 10 May 2012 (UTC)

Emperor is right.
If we see the texts written on the wall of the tombs of Goguryeo, or the stele, we can know that Goguryean rulers used the title, Taewang. So Emperor Gwanggaeto is right. — Preceding unsigned comment added by World historia (talk • contribs) 10:45, 10 May 2012 (UTC) World historia (talk) 08:19, 17 May 2012 (UTC)
 * No, You are Wrong. The academia, including Korean, consider Goguryeo as Kingdom, Not Empire.--121.167.254.156 (talk) 11:24, 17 May 2012 (UTC)

Please argue with historical evidences, not what academy under colonialism. If you cannot, accept the title, Taewang. — Preceding unsigned comment added by 222.101.9.93 (talk) 22:54, 16 July 2012 (UTC)

The citations listed that supposedly equate T'aewang with Emperor do not actually support this assertion. Why are people translating Taewang as emperor? Kojong used t'aewang also, before upgrading his title again to hwangjae (which is actually emperor). — Preceding unsigned comment added by Konamaiki (talk • contribs) 18:11, 17 May 2018 (UTC)

Recent page move
I undid the recent page move from Gwanggaeto the Great to Emperor Gwanggaeto per WP:COMMONNAME. "Emperor Gwanggaeto" has only two hits with Google Books and only one with Google Scholar.

--Kusunose 02:41, 11 May 2012 (UTC)

Requested move

 * The following discussion is an archived discussion of a requested move. Please do not modify it. Subsequent comments should be made in a new section on the talk page. No further edits should be made to this section.

The result of the move request was: not moved. Favonian (talk) 10:04, 22 May 2012 (UTC)

Gwanggaeto the Great → Emperor Gwanggaeto – This is processual request. This page had been titled Gwanggaeto the Great more than three years and before that, Gwanggaeto the Great of Goguryeo. Recently the page was moved twice to Emperor Gwanggaeto. As I thought thw new title is agaist established guidelines (see my reasoning below) and controversial, I undid them per WP:STATUSQUO and now initiating discussion per WP:RM. The reason for the move, as I see from above sections ( and ), is that his title "Taewang" should be translated as "Emperor". --Kusunose 06:07, 15 May 2012 (UTC)
 * Oppose First, the new title seems not WP:COMMONly used by reliable sources (see ). Even with the Google Web Search, "Emperor Gwanggaeto" gets about 1000 pages, while "Gwanggaeto the Great" returns millions of pages. Second, whether or not "Taewang" should be translated as "Emperor" in English, per Naming conventions (Korean), artile titles for Korean royals are not prefixed with one's title, "King" or "Emperor". --Kusunose 06:07, 15 May 2012 (UTC)
 * Comment. The subject is generally given as "King Kwanggaet'o". See Kim's The History of Korea (2005), Hwang's A History of Korea (2010), or Seth's A Concise History of Korea (2010). Kauffner (talk) 15:39, 15 May 2012 (UTC)
 * Oppose per following Google Book Search.
 * "King Gwanggaeto" -"King Gwanggaeto the great" -LLC -Wikipedia 136
 * "King Gwanggaeto the great" -LLC -Wikipedia 59
 * "Gwanggaeto the great" -"King Gwanggaeto the great" -LLC -Wikipedia 43
 * "Emperor Gwanggaeto" -LLC -Wikipedia 0
 * ―― Phoenix7777 (talk) 11:31, 18 May 2012 (UTC)
 * You can only access Google. Since it is Korean history, you should search korean information in naver. If you find 광개토태왕 and 광개토대왕, 광개토태왕 is overwhelmingly more. 222.101.9.93 (talk) 22:29, 20 May 2012 (UTC)
 * This is English Wikipedia. Per WP:USEENGLISH, we should follow the established English usage, not Korean. And do not remove comments made by other editors. See WP:TALK. --Kusunose 01:06, 21 May 2012 (UTC)

 * Oppose. 태왕, taewang, does not translate as "Emperor" (황제). We have a (stub) article on Taewang, and the translation is relevant since renaming the article to "Emperor" contradicts the information on that page, which specifically (and correctly) states that it does not mean that. --Tyrannus Mundi (talk) 05:03, 21 May 2012 (UTC)
 * As the lawyers say, this is a distinction without a difference. Taewang was understood as a title equivalent to that of the Chinese emperor (wangtae). "The great" suggests a comparison with other rulers of the same dynasty. All the Goguryeo kings held the title taewang. In any case, the article title should correspond to the way the subject is referred to in the best available English-language sources. What he is called in Korean should not have anything to do with it. Kauffner (talk) 23:00, 21 May 2012 (UTC)
 * Oppose. Using "Emperor" or "King" before the monarch's name is uncommon in Wikipedia. Reigen (talk) 14:57, 21 May 2012 (UTC)
 * The above discussion is preserved as an archive of a requested move. Please do not modify it. Subsequent comments should be made in a new section on this talk page. No further edits should be made to this section.

Move protected
Since people seem to be move-warring in the middle of an RM, I've move-protected the page for a while. If I see it resume upon expiration of the move protection, I'll block whoever it is. Use this time to sort out the RM, and note that my protection isn't an endorsement of the this title; I merely think that a page should stay in one place during an RM, and this is where the RM was started. The Blade of the Northern Lights ( 話して下さい ) 03:08, 21 May 2012 (UTC)

Request for comment
There has been an edit war here that includes multiple anonymous editors inserting the same material. The edit seems to revolve around Korean v. Chinese versions of history. Is one side more accurate, or can the two versions be brought together somehow? Thanks, Aristophanes 68   (talk)  19:56, 7 May 2017 (UTC)

Threaded discussion

 * Comment Can you please phrase the RfC question more specifically? For example, by giving us two or three different versions to discuss? Seraphim System  ( talk ) 04:38, 14 May 2017 (UTC)
 * Comment Your wording seems asserting that all Korean people are thinking the same, and all Chinese people are thinking the same. This is not factual. Moreover, this gives the impression that you are thinking that all these Eastern people are only creating trouble in your great Western encyclopedia. Let me disagree. Pldx1 (talk) 10:12, 14 May 2017 (UTC)
 * Obviously, I wasn't implying that all Koreans and all Chinese think the same way, but that the arguments seems to revolve around whether to describe the events and people of Goguryeo as basically Korean or as part of Chinese history. Aristophanes 68   (talk)  02:38, 15 May 2017 (UTC)

Comment: Let's say that Version A is the original. Version B is the one with all the stuff about tributary states.
 * Rephrased, Part 1: Should the lead read "was the nineteenth monarch of the Han Chinese tributary state of Goguryeo which sent yearly tribute to the Emperor of China" or "was the nineteenth monarch of Goguryeo"? Aristophanes 68   (talk)  02:38, 15 May 2017 (UTC)
 * Part 2: Should the lead read " Gwanggaeto's imperial reign title meant that Goguryeo was on equal standing as an empire with the imperial dynasties in China" or "Gwanggaeto's imperial reign title of "Taewang" was an unsuccessful attempt by the Goguryeo king to gain equal standing and status with the supreme rule of the Han emperor of China, who was regarded as the Son of Heaven or 'ruler of the whole universe.' After many requests by the Korean king the Emperor of China rejected his attempt and subsequently regarded the Korean leader as a subordinate regional king of the Korean peninsula and well within the domain of the Empire of China. The Korean monarch's insistence on using the sacred and restricted coat of arms of the five-claw dragon, a symbol reserved exclusively for the Emperor of China, resulted in the Chinese emperor sending a military invasion that conquered and re-established Korea as one of the Empire of China's subordinate tributary states"?  Aristophanes 68   (talk)  02:40, 15 May 2017 (UTC)

1) Version A is backed by citations. I opened and examined the citations and they support Version A. I suggest everyone else check too. Version A is supported by citations therefore it is appropriate.

2) Version B is NOT backed by citations. Version B replaces and messes up Version A (which is supported by citations) and is unrelated to the citations of the passages it replaces. Therefore Version B is inappropriate. The fact is that Version A is supported by citations and Version B is not and that should be the end of discussion on which version is acceptable. However, there's more problems with Version B.

3) Why is there a link to "History of Science and Technology in China"? What does THAT have to do with any of this?

4) Version B's long passage about Cao Wei and Goguryeo is anachronistic and happened more than a century before Gwanggaeto was even born. Yet that passage was added to Gwanggaeto's reign which makes that entire passage misleading and completely false.

IMO it's very clear that Version B is problematic and not appropriate. YB92 (talk) 23:02, 15 May 2017 (UTC)

Comment You might want to consider that 'Han China' did not even exist at the time of Gwanggaeto.... Wandrative (talk) 20:14, 2 October 2017 (UTC)

External links modified
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minor fix
but was defeated both times

change to:

but were defeated both times68.40.122.133 (talk) 16:06, 30 December 2017 (UTC)

Semi-protected edit request on 23 April 2023
westen = western 2603:8000:D300:D0F:C066:DFF9:D743:49D7 (talk) 22:07, 23 April 2023 (UTC)
 * ✅ Tollens (talk) 22:23, 23 April 2023 (UTC)

title: Talk:Gwanggaeto the Great


text:
Mineralocorticoid

Mineralocorticoids are a class of corticosteroids, which in turn are a class of steroid hormones. Mineralocorticoids are produced in the adrenal cortex and influence salt and water balances (electrolyte balance and fluid balance). The primary mineralocorticoid is aldosterone.

Physiology
The name mineralocorticoid derives from early observations that these hormones were involved in the retention of sodium, a mineral. The primary endogenous mineralocorticoid is aldosterone, although a number of other endogenous hormones (including progesterone and deoxycorticosterone) have mineralocorticoid function.

Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of potassium in the principal cells of the cortical collecting tubule and active secretion of protons via proton ATPases in the lumenal membrane of the intercalated cells of the collecting tubule. This in turn results in an increase of blood pressure and blood volume.

Aldosterone is produced in the zona glomerulosa of the cortex of the adrenal gland and its secretion is mediated principally by angiotensin II but also by adrenocorticotrophic hormone (ACTH) and local potassium levels.

Mode of action
The effects of mineralocorticoids are mediated by slow genomic mechanisms through nuclear receptors as well as by fast nongenomic mechanisms through membrane-associated receptors and signaling cascades.

Genomic mechanisms
Mineralocorticoids bind to the mineralocorticoid receptor in the cell cytosol, and are able to freely cross the lipid bilayer of the cell. This type of receptor becomes activated upon ligand binding. After a hormone binds to the corresponding receptor, the newly formed receptor-ligand complex translocates into the cell nucleus, where it binds to many hormone response elements (HREs) in the promoter region of the target genes in the DNA.

The opposite mechanism is called transrepression. The hormone receptor without ligand binding interacts with heat shock proteins and prevents the transcription of targeted genes.

Aldosterone and cortisol (a glucosteroid) have similar affinity for the mineralocorticoid receptor; however, glucocorticoids circulate at roughly 100 times the level of mineralocorticoids. An enzyme exists in mineralocorticoid target tissues to prevent overstimulation by glucocorticoids. This enzyme, 11-beta hydroxysteroid dehydrogenase type II (Protein:HSD11B2), catalyzes the deactivation of glucocorticoids to 11-dehydro metabolites. Licorice is known to be an inhibitor of this enzyme and chronic consumption can result in a condition known as pseudohyperaldosteronism.

Pathophysiology
Hyperaldosteronism (the syndrome caused by elevated aldosterone) is commonly caused by either idiopathic adrenal hyperplasia or by an adrenal adenoma. The two main resulting problems:

 * 1) Hypertension and edema due to excessive Na+ and water retention.
 * 2) Accelerated excretion of potassium ions (K+). With extreme K+ loss there is muscle weakness and eventually paralysis.

Hypoaldosteronism (the syndrome caused by underproduction of aldosterone) leads to the salt-wasting state associated with Addison's disease, although classical congenital adrenal hyperplasia and other disease states may also cause this situation. Acute underproduction (hemorrhagic adrenalitis) is often life-threatening.

Pharmacology

An example of a synthetic mineralocorticoid is fludrocortisone (Florinef).

Important antimineralocorticoids are spironolactone and eplerenone.

title: Mineralocorticoid


text:
Harald Tandrup

Harald Tandrup (31 January 1874 in Copenhagen – 10 May 1964) was a Danish writer. He used the pseudonyms Claus Colding or Klavs Kolding. His first novel was entitled Ain-Mokra and appeared 1900. He also wrote Reluctant Prophet (first U.S. edition in 1939). In 1946 he was excluded from the Danish Writer's Association (Danske Dramatikeres Forbund).

title: Harald Tandrup


text:
Talk:Winchester Mystery House

Improving the page
I am in the process of overhauling this page as I have found citation links that are broken, the citation does not say what is said on the page, or the citations were from unreliable sources. Dates have been found to be incorrect and information false according to reliable sources. I have also found some new information which will be added. I hope to be finished by the end of August. I look forward to feedback at that time.Hippopotenuse72 (talk) 19:13, 10 August 2022 (UTC)

 * Thank you for this! There are still a lot of citations that are needed for this article if anyone wants to help. This page still needs quite a bit of cleanup and citations. MMiller324 (talk) 01:20, 3 September 2022 (UTC)
 * What an interesting rewrite...but more work than I anticipated. I have published and look forward to seeing people make it better by correcting my grammar etc. My next project is to rewrite Sarah Winchester's page. Hopefully it won't take me as long. Hippopotenuse72 (talk) 03:00, 10 September 2022 (UTC)

Edit war
User Historybuff 5674 is reverting well-sourced edits and replacing them with a copy and paste of this website I am not sure how to request an admin. Please help. Thank you Hippopotenuse72 (talk) 00:30, 15 September 2022 (UTC)
 * I have blocked that editor for 72 hours. Let me know if the disruption resumes, and I will pageblock them from this article. Cullen328 (talk) 00:39, 15 September 2022 (UTC)
 * Thank you!! Hippopotenuse72 (talk) 01:15, 15 September 2022 (UTC)

Number 13
''There are many modern references to Winchester's apparent love of the number thirteen. The chandeliers hold thirteen candles, there are thirteen bathrooms, thirteen windows, thirteen ceiling panels, and thirteen coat hooks in the home. However these items were added to the home after her death and the first mention of her apparent love of thirteen was recorded in 1929, seven years after her death.''

That's just not believable. There's only 13 windows in this huge house? Valgrus Thunderaxe (talk) 07:49, 18 October 2022 (UTC)

 * Thirteen in one room. The owners of the home are cherry-picking in order to find hits to the number 13. Sgerbic (talk) 20:50, 18 October 2022 (UTC)

 * But is says thirteen in the house. Valgrus Thunderaxe (talk) 06:15, 19 October 2022 (UTC)

 * Tour guides have described feelings of being watched I had to laugh when I read this. - LuckyLouie (talk) 21:41, 18 October 2022 (UTC)
 * HAHA - That is funny. About the windows - obviously there are not only 13 windows in the entire house, but in some rooms. The rooms that the tour guides point out as having 13 windows, which of course means they have 13 windows. Someone could take a whack at improving that bit if they wanted to. Words can be funny things. Sgerbic (talk) 17:26, 19 October 2022 (UTC)
 * If there is an easily accessible source that clarifies the individual room window count vs. total house window count I would fix it. Found 'em and fixed it. - LuckyLouie (talk) 17:38, 19 October 2022 (UTC)

Official Source Updates
Hi All! I will be making edits to this page due to some incorrect & inaccurate information. This page is the "Winchester Mystery House" page which should only be touching on the house as an official historic landmark in the state of California. I am an employee at The Winchester Mystery House and many of the recent edits were made using one of the only biographies written about Sarah Winchester. Many of these sections that have been added would be better fitted for the Sarah Winchester page. The edits and the biography do not include information from our archives and discoveries the Winchester Mystery House staff has found over the 100 years of operation. The author did not interview anyone affiliated with the house and many of the edits to this page are opinions.

For over 100 years, the Winchester Mystery House has been sharing Sarah's life story, the odd design features of the home and the rumors, legend and lore that plagued her during her lifetime. We are very respectful of Sarah and her home, and take great pride in what we do. We invest millions of dollars and countless hours of labor to upkeep and restore her home and are an official city, state and national historic landmark. We employ an Historian on the estate who aids our tour department in creating and updating our tours when new information emerges within the home or Sarah's story.

Any claims of the paranormal that have been documented for the last 100 years by visitors, paranormal investigators, mediums, psychics and caretakers of the estate are presented as claims, not fact.

The fact is that stories of seances and spiritualism appeared in newspapers during Sarah's lifetime. No personal correspondence or articles have been found from Sarah denying or confirming her beliefs or these rumors.

Evidence of the life after death, the paranormal or supernatural has not and can not be proven nor disproven. We ask guests, fans and readers to visit the estate and come to their own conclusions about why Sarah built the house the way she did. Ameliar029 (talk) 19:29, 25 October 2022 (UTC)

 * This page has no single author, it's been written by many Wikipedia volunteer editors over the past 19 years. As an employee of the house your talk page input on inaccuracies and omissions is in the article is welcomed, but Wikipedia conflict of interest guidelines would discourage your from editing the article directly, and particularly adding content in a promotional tone. I've left a note on your talk page regarding the conflict of interest policy.
 * Wikipedia generally doesn't take a "can not be proven nor disproven" middle ground on a question such as whether ghosts exist, per WP:PSEUDOSCIENCE, although ghostly stories can be presented in context in an article such as this one. --Belbury (talk) 20:39, 25 October 2022 (UTC)
 * Hi @Belbury! Thank you for your guidance. Our primary concern is the phrase "It is sometimes claimed to be one of the “most haunted places in the world”, however there is no evidence to support this belief. Much of the lore regarding the Winchester House and its owner is fanciful, unverified, and often proven false." - as you mentioned wikipedia does not generally take a proven or disproving stance but this line remains unchallenged by you and other contributors. 100s of articles have been written over the years listing Winchester Mystery House as one of the most haunted places in the world - would it be best to site these articles in order to keep it fair? Thank you! Ameliar029 (talk) 20:50, 25 October 2022 (UTC)
 * As Belbury mentioned, Wikipedia can't give credibility to the supernatural per WP:FRINGE. Claims of the house being "most haunted in the world" etc. are WP:SENSATIONAL and are not given WP:UNDUE weight. The lead section summarizes what has been cited in the article body, and accurately identifies various legends, lore, and hyperbolic claims as factually untrue or unsubstantiated. Also, please keep WP:COI on mind. “we ask guests, fans and readers to visit the estate and come to their own conclusions about why Sarah built the house the way she did”…Also see WP:NOTADVERTISING. - LuckyLouie (talk) 21:04, 25 October 2022 (UTC)
 * Hi @LuckyLouie! As stated in my previous post earlier, this page should only be touching on the house as an official historic landmark in the state of California as it has in the past. The sections you are referring to in the article are cited by one of the only Sarah Winchester biographies that has been written in which the biographer did not include information from our archives and discoveries the Winchester Mystery House staff has found over the 100 years of operation. To comply with the WP:FRINGE I suggest we remove any mentions of the paranormal claims from the article that cannot be proved nor disproved. Thoughts? Thanks! Ameliar029 (talk) 23:33, 25 October 2022 (UTC)
 * The way WP:FRINGE policy works is that we give the most weight to independent expert opinion on a topic. In the case of topics that feature marginalized viewpoints, we lean towards the mainstream. And mainstream scientific consensus rejects explanations that embrace the paranormal, supernatural, ghosts, demons, etc. So in this case, we have Joe Nickell, Mary Jo Ignoffo, Brian Dunning, Katie Dowd, Colin Dickey, etc. writing in line with that scientific consensus, and also as experts who are (importantly) independent of monetary incentive to promote mystery, drama, superstition, hype, etc. These experts analysis and criticism of the various claims made about the house are quite relevant. And since Wikipedia is an encyclopedia, it doesn't remove well-sourced criticism of a subject just because it might be bad for the subject's business. However I do agree that "Legend & lore" was an improvement as a section title. Thanks. - LuckyLouie (talk) 15:40, 26 October 2022 (UTC)

 * "Evidence of the life after death, the paranormal or supernatural has not and can not be proven nor disproven." Per Fringe it does not work this way. Also, evidence of smurfs can't be proven or disproven by your same logic. I hope we can both agree that to state that these same statements are equal (smurfs might or might not exist) is a silly statement. Let's just get this clear right off the bat Ameliar029 no serious Wikipedian is going to allow this false equivalent to exist on this page. Sgerbic (talk) 23:46, 25 October 2022 (UTC)
 * Hi @Sgerbic - In my last comment I suggested we remove all mentions of paranormal claims off of this article to keep it solely historical in regards to complying with Fringe. Thoughts? Thanks! Ameliar029 (talk) 23:53, 25 October 2022 (UTC)
 * I don't think that will work Ameliar as the researchers are writing ABOUT the paranormal claims and responding to them. The researchers are the ones with the notability, not the people making the paranormal claims. There would be no context to what the researchers have said if we remove the claims. Further, we don't allow Wikipedians to do original research and contact the house to write the page. That is NOT how Wikipedia works. To add in that it is a haunted house is promotional, the statement is inferring that haunting and ghosts are real, and the Winchester House is one of the "most haunted" like there is some kind of competition that can be evaluated. How could that be evaluated if there is no evidence showing that ghosts exist? We do allow opinions from scholars and researchers that are considered notable for those skills. The opinions are attributed to the source it comes from per Wikipedia policies. I would be willing to allow citations of those 100s of articles that have been written about the House being one of the most haunted places in the world as soon as we have real evidence of hauntings and ghosts within the consistence of science. At the moment, not seeing that evidence anywhere but at Joe's blog on ghosties sites and other websites that are clearly aimed at getting clicks and people to visit. I hope you understand Ameliar029, your statements here on talk seem to be aimed at protecting revenue and not just the history. You say that the staff has found a lot and it's in the archives, that won't do us any good until a researcher has evaluated those archives and written about them. We can't take your word for it, we don't use primary sources in this case. You said in your first statement that there is "no personal correspondence or articles have been found from Sarah denying or confirming her beliefs or these rumors." If there is none, then that is that. She didn't deny being a reptilian did she? Well, should be include that in the article and say she didn't denying being a reptilian? Sgerbic (talk) 00:09, 26 October 2022 (UTC)
 * I'm not understanding how you can say that you all are respectful of the House (with jump scares and a "terrifying journey thought the worlds most haunted home") and only want to protect the history. I've been on the tour many times and it's clearly paranormal focused. It has gotten a lot better the last few years, but the "some people say ..." is still there. But with a straight face (well I can't see your face) you are trying to tell us that the paranormal isn't a focus when every Halloween there is a "Halloween Haunt" and you allow people like James Van Praagh there to do $250 psychic events?. I see a new tour has just been added 'Walk with spirits" and "Unhinged: Nightshades curse" - "13 select nights". Come on now. Sgerbic (talk) 00:22, 26 October 2022 (UTC)

I tagged the "most haunted" section as "vague."
"It is sometimes claimed to be one of the “most haunted places in the world”, but there is no evidence to support this belief. Much of the lore regarding the Winchester House and its owner is fanciful, unverified, and often provably false."

Calling something a "most haunted place" could either mean it's literally haunted, or that there's enough folklore surrounding it to be culturally significant. If it's the latter, the Winchester House probably meets that criterion. If it's the former, then the scientific stance on that should be so obvious I'm not sure it bears repeating unless a specific claim is being made (e.g., that organ music can be heard in the house). It also implies that these claims were worth serious consideration by researchers, something that definitely would require a citation.

It's also just really vague. "Much of the lore?" How much and what counts as "lore?"

This is kind of trivial, I know, but it just struck me as odd and kind of humorous to be reminded that ghosts aren't real in an encyclopedia article about a house. 2603:7081:1603:A300:5D2A:5E39:2A96:6A62 (talk) 22:28, 22 July 2023 (UTC)

 * Read WP:LEAD and then WP:LEADFOLLOWSBODY, then see Winchester_Mystery_House citation numbers 10,17, 27 and 28. - LuckyLouie (talk) 22:51, 22 July 2023 (UTC)

title: Talk:Winchester Mystery House


text: Talk:Seong of Baekje

title: Talk:Seong of Baekje


text:
Linux Mark Institute

The Linux Mark Institute (LMI, fully "LMI Oregon, LLC" ) is an organization which administers the "Linux" trademark on behalf of Linus Torvalds for computer software which includes the Linux kernel, computer hardware utilizing Linux-based software, and for services associated with the implementation and documentation of Linux-based products.

Trademark
The Linux trademark is owned by Linus Torvalds in the U.S., Germany, the E.U., and Japan for "Computer operating system software to facilitate computer use and operation". The assignment of the trademark to Torvalds occurred after a lawsuit against attorney William R. Della Croce Jr., of Boston, who had registered the trademark in the US in September 1995 and began in 1996 to send letters to various Linux distributors, demanding ten percent of royalties from sales of Linux products. A petition against Della Croce's practices was started, and in early 1997, WorkGroup Solutions, Yggdrasil, Linux Journal, Linux International, and Torvalds appealed the original trademark assignment as "fraudulent and obtained under false pretenses". By November, the case was settled and Torvalds owned the trademark.

History
LMI originally charged a nominal sublicensing fee for use of the Linux name as part of trademarks, but later changed this in favor of offering a free, perpetual worldwide sublicense.

LMI was headquartered in Monterey, California until at least 2005. Since at least 2009 it was headquartered in Beaverton, Oregon.

title: Linux Mark Institute


text:
Talk:Munmu of Silla

Low-intensity edit war?
It seems for months theres been an ongoing low-intensity edit war between various editors on the title of Munmu, I feel this should be addresesed here. Sunnyediting99 (talk) 22:06, 8 June 2024 (UTC)

 * There is this one guy who is constantly changing a lot of different articles concerning monarchs of Silla by adding the title "the great" indiscriminately. This has been occurring with kim Yu-shin, Muyeol of Silla, Jinheung of Silla, and several others. With no explanation source or otherwise. The guy started quite a while back and has been trying, for some reason, to change most monarchs to "the great" its not important but it very strange. He been banned before and this page in particular has been protected because he has been circumventing the ban. Sanctusune (talk) 23:03, 8 June 2024 (UTC)
 * We might need to put in a page protection at this rate then Sunnyediting99 (talk) 12:02, 9 June 2024 (UTC)
 * Sanctusune since you know more about this, perhaps you submit it? Sunnyediting99 (talk) 21:46, 10 June 2024 (UTC)
 * sure I can do that. Sanctusune (talk) 22:19, 12 June 2024 (UTC)
 * actually, there hasn't been a lot of current vandalism, but if it starts up again I will certainly do it. Sanctusune (talk) 22:26, 12 June 2024 (UTC)

title: Talk:Munmu of Silla


text:
Muscle memory

Muscle memory is a form of procedural memory that involves consolidating a specific motor task into memory through repetition, which has been used synonymously with motor learning. When a movement is repeated over time, the brain creates a long-term muscle memory for that task, eventually allowing it to be performed with little to no conscious effort. This process decreases the need for attention and creates maximum efficiency within the motor and memory systems. Muscle memory is found in many everyday activities that become automatic and improve with practice, such as riding bikes, driving motor vehicles, playing ball sports, typing on keyboards, entering PINs, playing musical instruments, poker, martial arts, swimming, dancing, and drawing.

History
The origins of research for the acquisition of motor skills stem from philosophers such as Plato, Aristotle and Galen. After the break from tradition of the pre-1900s view of introspection, psychologists emphasized research and more scientific methods in observing behaviours. Thereafter, numerous studies exploring the role of motor learning were conducted. Such studies included the research of handwriting, and various practice methods to maximize motor learning.

Retention
The retention of motor skills, now referred to as muscle memory, also began to be of great interest in the early 1900s. Most motor skills are thought to be acquired through practice; however, more observation of the skill has led to learning as well. Research suggests we do not start off with a blank slate with regard to motor memory although we do learn most of our motor memory repertoire during our lifetime. Movements such as facial expressions, which are thought to be learned, can actually be observed in children who are blind; thus there is some evidence for motor memory being genetically pre-wired.

In the early stages of empirical research of motor memory Edward Thorndike, a leading pioneer in the study of motor memory, was among the first to acknowledge learning can occur without conscious awareness. One of the earliest and most notable studies regarding the retention of motor skills was by Hill, Rejall, and Thorndike, who showed savings in relearning typing skills after a 25-year period with no practice. Findings related to the retention of learned motor skills have been continuously replicated in studies, suggesting that through subsequent practice, motor learning is stored in the brain as memory. This is why performing skills such as riding a bike or driving a car are effortlessly and 'subconsciously' executed, even if someone had not performed these skills in a long period of time.

Motor behavior
When first learning a motor task, movement is often slow, stiff and easily disrupted without attention. With practice, execution of motor task becomes smoother, there is a decrease in limb stiffness, and muscle activity, necessary to the task, is performed without conscious effort.

Muscle memory encoding
The neuroanatomy of memory is widespread throughout the brain; however, the pathways important to motor memory are separate from the medial temporal lobe pathways associated with declarative memory. As with declarative memory, motor memory is theorized to have two stages: a short-term memory encoding stage, which is fragile and susceptible to damage, and a long-term memory consolidation stage, which is more stable. The memory encoding stage is often referred to as motor learning, and requires an increase in brain activity in motor areas as well as an increase in attention. Brain areas active during motor learning include the motor and somatosensory cortices; however, these areas of activation decrease once the motor skill is learned. The prefrontal and frontal cortices are also active during this stage due to the need for increased attention on the task being learned.

The main area involved in motor learning is the cerebellum. Some models of cerebellar-dependent motor learning, in particular the Marr-Albus model, propose a single plasticity mechanism involving the cerebellar long-term depression (LTD) of the parallel fiber synapses onto Purkinje cells. These modifications in synapse activity would mediate motor input with motor outputs critical to inducing motor learning. However, conflicting evidence suggests that a single plasticity mechanism is not sufficient and a multiple plasticity mechanism are needed to account for the storage of motor memories over time. Regardless of the mechanism, studies of cerebellar-dependent motor tasks show that cerebral cortical plasticity is crucial for motor learning, even if not necessarily for storage.

The basal ganglia also play an important role in memory and learning, in particular in reference to stimulus-response associations and the formation of habits. The basal ganglia-cerebellar connections are thought to increase with time when learning a motor task.

Muscle memory consolidation
Muscle memory consolidation involves the continuous evolution of neural processes after practicing a task has stopped. The exact mechanism of motor memory consolidation within the brain is controversial. However, most theories assume that there is a general redistribution of information across the brain from encoding to consolidation. Hebb's rule states that "synaptic connectivity changes as a function of repetitive firing." In this case, that would mean that the high amount of stimulation coming from practicing a movement would cause the repetition of firing in certain motor networks, presumably leading to an increase in the efficiency of exciting these motor networks over time.

While the exact location of muscle memory storage is not known, studies have suggested that it is the inter-regional connections that play the most important role in advancing motor memory encoding to consolidation, rather than decreases in overall regional activity. These studies have shown a weakened connection from the cerebellum to the primary motor area with practice, it is presumed, because of a decreased need for error correction from the cerebellum. However, the connection between the basal ganglia and the primary motor area is strengthened, suggesting the basal ganglia play an important role in the motor memory consolidation process.

Strength training and adaptations
When participating in any sport, new motor skills and movement combinations are frequently being used and repeated. All sports require some degree of strength, endurance training, and skilled reaching in order to be successful in the required tasks. Muscle memory related to strength training involves elements of both motor learning, described below, and long-lasting changes in the muscle tissue.

Evidence has shown that increases in strength occur well before muscle hypertrophy, and decreases in strength due to detraining or ceasing to repeat the exercise over an extended period of time precede muscle atrophy. To be specific, strength training enhances motor neuron excitability and induces synaptogenesis, both of which would help in enhancing communication between the nervous system and the muscles themselves. However, neuromuscular efficacy is not altered within a two-week time period following cessation of the muscle usage; instead, it is merely the neuron's ability to excite the muscle that declines in correlation with the muscle's decrease in strength. This confirms that muscle strength is first influenced by the inner neural circuitry, rather than by external physiological changes in the muscle size.

Previously untrained muscles will acquire newly formed nuclei through the fusion of satellite cells preceding hypertrophy. Subsequent detraining will result in atrophy and the loss of myo-nuclei. While it was long believed that a muscle memory effect related to myo-nuclei permanence existed, current studies establish that during detraining, myo-nuclei will be lost.

Reorganization of motor maps within the cortex are not altered in either strength or endurance training. However, within the motor cortex, endurance induces angiogenesis within as little as three weeks to increase blood flow to the involved regions. In addition, neurotropic factors within the motor cortex are upregulated in response to endurance training to promote neural survival.

Skilled motor tasks have been divided into two distinct phases: a fast-learning phase, in which an optimal plan for performance is established, and a slow-learning phase, in which longer-term structural modifications are made on specific motor modules. Even a small amount of training may be enough to induce neural processes that continue to evolve even after the training has stopped, which provides a potential basis for consolidation of the task. In addition, studying mice while they are learning a new complex reaching task, has found that "motor learning leads to rapid formation of dendritic spines (spinogenesis) in the motor cortex contralateral to the reaching forelimb". However, motor cortex reorganization itself does not occur at a uniform rate across training periods. It has been suggested that the synaptogenesis and motor map reorganization merely represent the consolidation, and not the acquisition itself, of a specific motor task. Furthermore, the degree of plasticity in various locations (namely motor cortex versus spinal cord) is dependent on the behavioural demands and nature of the task (i.e., skilled reaching versus strength training).

Whether strength or endurance related, it is plausible that the majority of motor movements would require a skilled moving task of some form, whether it be maintaining proper form when paddling a canoe, sitting with a neutral posture, or bench pressing a heavier weight. Endurance training assists the formation of these new neural representations within the motor cortex by up regulating neurotropic factors that could enhance the survival of the newer neural maps formed due to the skilled movement training. Strength training results are seen in the spinal cord well before any physiological muscular adaptation is established through muscle hypertrophy or atrophy. The results of endurance and strength training, and skilled reaching, therefore, combine to help each other maximize performance output.

More recently, research has suggested that epigenetics may play a distinct role in orchestrating a muscle memory phenomenon Indeed, previously untrained human participants experienced a chronic period of resistance exercise training (7 weeks) that evoked significant increases in skeletal muscle mass of the vastus lateralis muscle, in the quadriceps muscle group. Following a similar period of physical in-activity (7 weeks), where strength and muscle mass returned to baseline, participants performed a secondary period of resistance exercise. Importantly, these participants adapted in an enhanced manner, whereby the amount of skeletal muscle mass gained was greater in the second period of muscle growth than the first, suggesting a muscle memory concept. The researchers went on to examine the human epigenome in order to understand how DNA methylation may aid in creating this effect. During the first period of resistance exercise, the authors identify significant adaptations in the human methylome, whereby over 9,000 CpG sites were reported as being significantly hypomethylated, with these adaptations being sustained during the subsequent period of physical in-activity. However, upon secondary exposure to resistance exercise, a greater frequency of hypomethylated CpG sites was observed, where over 18,000 sites reported as being significantly hypomethylated. The authors went on to identify how these changes altered the expression of relevant transcripts, and subsequently correlated these changes with adaptations in skeletal muscle mass. Collectively, the authors conclude that skeletal muscle mass and muscle memory phenomenon is, at least in part, modulated due to changes in DNA methylation. Further work is now needed to confirm and explore these findings.

Fine motor memory
Fine motor skills are often discussed in terms of transitive movements, which are those done when using tools (which could be as simple as a tooth brush or pencil). Transitive movements have representations that become programmed to the premotor cortex, creating motor programs that result in the activation of the motor cortex and therefore the motor movements. In a study testing the motor memory of patterned finger movements (a fine motor skill) it was found that retention of certain skills is susceptible to disruption if another task interferes with one's motor memory. However, such susceptibility can be reduced with time. For example, if a finger pattern is learned and another finger pattern is learned six hours later, the first pattern will still be remembered. But attempting to learn two such patterns one immediately after the other could cause the first one to be forgotten. Furthermore, the heavy use of computers by recent generations has had both positive and negative effects. One of the main positive effects is an enhancement of children's fine motor skills. Repetitive behaviors, such as typing on a computer from a young age, can enhance such abilities. Therefore, children who learn to use computer keyboards at an early age could benefit from the early muscle memories.

Music memory
Fine motor skills are very important in playing musical instruments. It was found that muscle memory is relied on when playing the clarinet, specifically to help create special effects through certain tongue movements when blowing air into the instrument.

Certain human behaviours, especially actions like the finger movements in musical performances, are very complex and require many interconnected neural networks where information can be transmitted across multiple brain regions. It has been found that there are often functional differences in the brains of professional musicians, when compared to other individuals. This is thought to reflect the musician's innate ability, which may be fostered by an early exposure to musical training. An example of this is bimanual synchronized finger movements, which play an essential role in piano playing. It is suggested that bimanual coordination can come only from years of bimanual training, where such actions become adaptations of the motor areas. When comparing professional musicians to a control group in complex bimanual movements, professionals are found to use an extensive motor network much less than those non-professionals. This is because professionals rely on a motor system that has increased efficiency, and, therefore, those less trained have a network that is more strongly activated. It is implied that the untrained pianists have to invest more neuronal activity to have the same level of performance that is achieved by professionals. This, yet again, is said to be a consequence of many years of motor training and experience that helps form a fine motor memory skill of musical performance.

It is often reported that, when a pianist hears a well-trained piece of music, synonymous fingering can be involuntarily triggered. This implies that there is a coupling between the perception of music and the motor activity of those musically trained individuals. Therefore, one's muscle memory in the context of music can easily be triggered when one hears certain familiar pieces. Overall, long-term musical fine motor training allows for complex actions to be performed at a lower level of movement control, monitoring, selection, attention, and timing. This leaves room for musicians to focus attention synchronously elsewhere, such as on the artistic aspect of the performance, without having to consciously control one's fine motor actions.

Puzzle cube memory
Speed cubers use muscle memory when attempting to solve puzzle cubes, such as the Rubik's Cube, in the fastest possible time. Solving these puzzles in an optimally efficient manner requires the cube to be manipulated according to a set of complex algorithms. By building their muscle memory of each algorithm's movements, speed cubers can implement them at very fast speeds without conscious effort. This plays a role in major speedcubing methods such as Fridrich for the 3×3×3 Rubik's Cube and EG for the 2×2×2 Pocket Cube.

Gross motor memory
Gross motor skills are concerned with the movement of large muscles, or major body movements, such as those involved in walking or kicking, and are associated with normal development. The extent to which one exhibits gross motor skills depends largely on their muscle tone and the strength. In a study looking at people with Down Syndrome, it was found that the pre-existing deficits, with regard to verbal-motor performance, limits the individual's transfer of gross motor skills following visual and verbal instruction to verbal instruction only. The fact that the individuals could still exhibit two of the three original motor skills may have been a result of positive transfer in which previous exposure allows the individual to remember the motion, under the visual and verbal trial, and then later perform it under the verbal trial.

Learning in childhood
The way in which a child learns a gross motor skill can affect how long it takes to consolidate it and be able to reproduce the movement. In a study with preschoolers, looking at the role of self-instruction on acquiring complex gross motor chains using ballet positions, it was found that the motor skills were better learned and remembered with the self-instruction procedure over the no-self-instruction procedure. This suggests that the use of self-instruction will increase the speed with which a preschooler will learn and remember a gross motor skill. It was also found that once the preschoolers learned and mastered the motor chain movements, they ceased the use of self-instruction. This suggests that the memory for the movements became strong enough that there was no longer a need for self-instruction and the movements could be reproduced without it.

Effect of Alzheimer's disease
It has been suggested that consistent practice of a gross motor skill can help a patient with Alzheimer's disease learn and remember that skill. It was thought that the damage to the hippocampus may result in the need for a specific type of learning requirement. A study was created to test this assumption in which the patients were trained to throw a bean bag at a target. It was found that the Alzheimer's patients performed better on the task when learning occurred under constant training as opposed to variable. Also, it was found that gross motor memory in Alzheimer's patients was the same as that of healthy adults when learning occurs under constant practice. This suggests that damage to the hippocampal system does not impair an Alzheimer's patient from retaining new gross motor skills, implying that motor memory for gross motor skills is stored elsewhere in the brain. However there isn't much evidence provided on this.

Impairment
It is difficult to display cases of "pure" motor memory impairment because the memory system is so widespread throughout the brain that damage is not often isolated to one specific type of memory. Likewise, diseases commonly associated with motor deficits, such as Huntington's and Parkinson's disease, have a wide variety of symptoms and associated brain damage that make it impossible to pinpoint whether or not motor memory is in fact impaired. Case studies have provided some examples of how motor memory has been implemented in patients with brain damage.

As Edward S. Casey notes in Remembering, Second Edition: A Phenomenological Study, declarative memory, a process that involves an initial fragile learning period. "The activity of the past, in short, resides in its habitual enactment in the present."

Consolidation deficit
A recent issue in motor memory is whether or not it consolidates in a manner similar to declarative memory, a process that involves an initial fragile learning period that eventually becomes stable and less susceptible to damage over time. An example of stable motor memory consolidation in a patient with brain damage is the case of Clive Wearing. Clive has severe anterograde and retrograde amnesia owing to damage in his temporal lobes, frontal lobes, and hippocampi, which prevents him from storing any new memories and making him aware of only the present moment. However, Clive still retains access to his procedural memories, to be specific, the motor memories involved in playing the piano. This could be because motor memory is demonstrated through savings over several trials of learning, whereas declarative memory is demonstrated through recall of a single item. This suggests that lesions in certain brain areas normally associated with declarative memory would not affect motor memory for a well-learned skill.

Dysgraphia for the alphabet
Case study: 54-year-old man with known history of epilepsy This patient was diagnosed with a pure form of dysgraphia of letters, meaning he had no other speech or reading impairments. His impairment was specific to letters in the alphabet. He was able to copy letters from the alphabet, but he was not able to write these letters. He had previously been rated average on the Wechsler Adult Intelligence Scale's vocabulary subtest for writing ability comparative to his age before his diagnosis. His writing impairment consisted of difficulty remembering motor movements associated with the letters he was supposed to write. He was able to copy the letters, and also form images that were similar to the letters. This suggests that dysgraphia for letters is a deficit related to motor memory. Somehow there is a distinct process within the brain related to writing letters, which is dissociated from copying and drawing letter-like items.

title: Muscle memory


text:
Rafael Joseffy

Rafael Joseffy (July 3, 1852 – June 25, 1915) was a Hungarian Jewish pianist, teacher and composer.

Life
Rafael Joseffy was born in Hunfalu, Szepes County (now Huncovce, Slovakia) in 1852. His youth was spent in Miskolc, and he began his study of the piano there at the age of eight. He studied in Budapest with Friedrich Brauer, the teacher of Stephen Heller. In 1866, he went to Leipzig, where his teachers were Ignaz Moscheles and Ernst Ferdinand Wenzel. In 1868, he became a pupil of Karl Tausig in Berlin, remaining with him for two years. Later he spent two summers with Franz Liszt in Weimar. He made his debut in Berlin in 1872 and was immediately acclaimed as a master pianist of great brilliance.

He moved to the United States in 1879, where he lived in New York City. Joseffy made his American debut in New York in 1879, with an orchestra under Leopold Damrosch. He soon after played with the New York Philharmonic Orchestra, and subsequently made many appearances in New York and other American cities with Theodore Thomas and the Theodore Thomas Orchestra.

Joseffy was soloist for the inaugural concerts of the Chicago Symphony Orchestra on October 16 and 17, 1891, performing Tchaikovsky's First Piano Concerto with Thomas conducting at the Auditorium Theatre in Chicago.

Joseffy produced numerous popular compositions for the piano as well as editing works of Frédéric Chopin and other composers for G. Schirmer music publishers. Several of his songs were translated from German to English by Helen Tretbar.

Later in life he virtually retired from the concert platform and devoted his attention to teaching His students included the American composer and singer Florence Turner-Maley. He was a very reserved man. Henry Wolfsohn claimed to have offered Joseffy huge sums for concert tours but the pianist found concert life so severe upon his nerves that he would not accept. He preferred the smaller income of a teacher to the glare of the footlights. While in New York, he spent his summers in Tarrytown. He died in New York City in 1915, aged 62.

title: Rafael Joseffy


text:
Leipsic

Leipsic is a former English and very rare former French spelling for the German city of Leipzig.

Leipsic may also refer to:

Places in the United States

 * Leipsic, Delaware
 * Leipsic, Indiana
 * Leipsic, Ohio
 * West Leipsic, Ohio
 * Leipsic River, Delaware

People

 * Brendan Leipsic (born 1994), Canadian ice hockey player

title: Leipsic


text:
Talk:Saltaire

Feedback
To reply to ALargeElk's comment on peer review, your additions look excellent and perfectly NPOV to me, nice job. (With the caveat that as an American I don't know a thing about Saltaire, but Titus Salt is starting to remind me somewhat of Henry Ford in his philosophy.) - Hephaestos|§ 15:04, 16 Mar 2004 (UTC)

Thanks - I thought so, but it's nice to just hear it from someone else. --ALargeElk 15:07, 16 Mar 2004 (UTC)

A couple of contentious assertions
primarily to increase their profitability.

What is the basis of this assertion? He was a Christian as well as a capitalist, so concievably he could have been genuinely concerned. It's not the place of wikipedia to say which.

because he saw pubs as a breeding ground for dissent and the formation of trade unions.

This is contentious. It's not the reason he gave AIUI, though it may be the one reported in local (left-wing) papers. He provided alternative facilities; a library, etc, as listed. It was, I think, intended to improve the residents' ability to function as good Christians (e.g. by not getting into brawls or by drinking to excess). Mr. Jones 07:53, 10 Aug 2004 (UTC)

 * I've been bold. I've removed the entire section about Salt's motives, as I don't believe it's encyclopaedic. ColinFine 23:15, 25 July 2006 (UTC)

Another one... housing being much better than the slums of Bradford It's not clear to me in what way the houses are better than the Victorian housing in Bradford. In fact I would suggest that the houses in Bradford were generally larger and and with more space around them. Granted, Salt provided additional amenities... Any other opinions... Nick Watts 12:51, 17 August 2007 (UTC)

Copley
The comparison with Copley is problematic as that entry currently has a date of 1874, ie later than Saltaire. The Saltaire article currently claims Copley came first. --Alan 10:32, 26 May 2006 (UTC)

 * I noticed this. I'm also dubious as to whether Ackroyden and Copley are actually different, or whether Ackroyden is in fact at Copley. ColinFine 23:15, 25 July 2006 (UTC)

Sir James Roberts
Sir James did not lose all his fortune as a result of the Russian Revolution. When he sold the company in 1920 it was for a very considerable sum. He died a wealthy man in 1935 Millbanks 21:14, 15 July 2007 (UTC)

Assessment comment
Substituted at 05:19, 30 April 2016 (UTC)

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title: Talk:Saltaire