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Talk:Prader–Willi syndrome

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Top picture doesn't match caption?
I don't know anything about PWS, but the top image doesn't seem to match the description. The description says "Patient with the syndrome showing characteristic facial appearance, with elongated face, prominent nose, and smooth philtrum", but the face doesn't seem elongated, nor does the philtrum appear smooth. —Preceding unsigned comment added by 67.101.149.175 (talk) 21:54, 30 September 2010 (UTC) This picture is inappropriate because we haven't respected the privacy of this person. This boy should have his eyes blacked out at least. — Preceding unsigned comment added by 24.83.172.133 (talk) 00:42, 13 May 2012 (UTC)

The first two pictures in this article are the wrong syndrome. They're patients with 22q11.2 deletion syndrome (you can see they have digital watermarks from 'Images in Paediatric Cardiology' and people with PWS don't have a lot of congenital heart disease). The 'tubular' nose and slightly simple ears are features of 22q11 DS. The original images are from: Digilio MC, Marino B, Capolino R, Dallapiccola B. Clinical manifestations of Deletion 22q11.2 syndrome (DiGeorge/Velo-Cardio-Facial syndrome). Images Paediatr Cardiol 2005;23:23-34 http://www.impaedcard.com/issue/issue23/digiliom/digiliom.htm Afry (talk) 00:21, 21 February 2011 (UTC)

Reviewing the article after a few years I can see someone has put back in the images of two patients with Deletion 22q11.2 syndrome (DiGeorge syndrome). I am going to remove them. They don't look like children with PWS and they clearly come from an published article on 22q11.2 deletion syndrome. It is a different genetic condition! Putting in the pictures of the wrong condition is confusing for readers and potentially distressing for patients/families! Afry (talk) 12:18, 4 September 2016 (UTC)

Is that appropriate?
In the treatment portion of the article, it reads:
 * Throughout their lives, the subject's food should literally be kept under lock and key, since the largest problem associated with the syndrome is severe obesity.

Food kept under lock and key? Does Prader-Willi syndrome cause an abnormal desire for unnecessary consumption of food? If not, is that not statement not offensive? I'm a skinny guy, but I'd imagine 100 million overweight Americans wouldn't be pleased if they read this. Baribeau 00:05, 29 March 2007 (UTC)
 * I don't know much about Prader-Willi syndrome, but on the documentary I watched called "Can't Stop Eating," two individuals with PW syndrome were followed with a camera crew. It seemed to me that the individuals family, and caretakers, kept them away from the kitchen as much as possible. Actually, the teenage boy was at a center where the kitchen was literally locked tight to prevent him from getting in. It might not be that far fetched because the appetite seems to be unbearable for those with PW syndrome. As for offending overweight people - I would hope that the 100 million overweight Americans (I being one of them) would understand the situation. a person with PW syndrome has an appetite that is far more extreme than an average overweight persons. PoeticXcontribs|undefined 03:01, 30 April 2007 (UTC)

Yes, PW syndrome does cause massive, excessive consumption of food, and it does literally need to be lock away from them. DocGratis 00:52, 3 June 2007 (UTC)

I heard somewhere that Prader willi victims are always under the idea that there starved near to death because of the lack of messeges from the stomach, —Preceding unsigned comment added by 92.11.23.20 (talk) 14:29, 17 August 2009 (UTC)

my brother had this syndrome and yes, the person with this syndrome does not know never feel the satisfaction of being full up. He/she will always feel the urge to eat. Also why did you bring Americans in this? btw I'm Irish —Preceding unsigned comment added by Paulandmomo1 (talk • contribs) 00:43, 16 August 2010 (UTC)

Individuals with PWS have little or no impulse control when it comes to food. Virtually their entire lives revolve around getting food, having food, thinking about food and eating food. PWS is a genetic and psychiatric disorder. Most individuals who are overweight have control over themselves (whether or not they choose to exercise that control). For people with PWS, the control is, and never will be there. They literally cannot help themselves...they require a great deal of assistance and support. Food cravings and eating can be managed with routine, structure and consistency, but it is a lifelong struggle. — Preceding unsigned comment added by 174.91.138.50 (talk) 03:38, 16 November 2011 (UTC)

This page is plagiarized
This page appears to be copied from genetests.org. I'll work on replacing it soon InvictaHOG 01:50, 11 October 2005 (UTC)

How about some kind of symptoms? Bihal 11:29, 17 April 2006 (UTC)
 * I just saw a little thing on CNN about this which attributes retardation to the disorder as well. i'll put it in Joeyramoney 00:27, 10 June 2006 (UTC)

Prader-Willi Syndrome in the media
How about some references here. The author seems to assume that we know what market "channel 4" services —Preceding unsigned comment added by Phreed100 (talk • contribs) 18:51, 9 June 2008 (UTC)

channel four did do a documentary on pws —Preceding unsigned comment added by Paulandmomo1 (talk • contribs) 00:48, 16 August 2010 (UTC)

Appropoiatness of the Picture in the Intro...
The caption reads "A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader-Willi syndrome." Presumed by who? If we don't have a reputable source making the assumption, we can't make that claim, and the picture needs to be replaced. Seeing as the condition has only been described since 1956, I'm finding this unlikely. I added the tags, please try to address this in a timely manner. 24.190.34.219 (talk) 16:30, 6 September 2009 (UTC)
 * Jawohl Kapitan 24.190.34.219! Try Google, the 3rd hit on page 6 of The Poetry of Genetics: On the Pitfalls of Popularizing Science. Feel free to sort the references out yourself.

Photo of PWS patient
The current picture showing a patient with PWS has the caption: "note the absence of typical PWS features". If this article is supposed to be informative, how about we try to find a picture of a patient that actually HAS the typical features? 147.8.62.99 (talk) 13:48, 8 February 2010 (UTC)
 * 12 years later, and that's the first thing I noticed about the article. The picture at the top has the eyes boxed out, so there is no picture showing facial features.  Why not remove both of them if they are not helpful? --2607:FEA8:FF01:4E54:B138:19EB:6403:95EC (talk) 01:19, 2 February 2022 (UTC)

Suffer from
It is inappropriate to say that individuals suffer from any disability. This assumes a variety of things of the individual with the disorder. People have disorders, they do not "suffer" from them and many individuals would find this terminology offensive. A disability can be defining and important to the person that has it.

People suffer from diseases, not disabilities. —Preceding unsigned comment added by 68.104.157.139 (talk) 14:13, 23 September 2010 (UTC)

 * This is political correctness.  I have a mild disability that gives me poor eyesight and makes it impossible for me to drive, in a culture where driving is expected.  I don't find the word "suffer" offensive, nor do I find the disability "defining and important" to me, just frustrating.   2001:558:6011:1:E592:162A:3D0B:1B42 (talk) 00:57, 2 April 2018 (UTC)

Society and Culture
"In Judas Strain, a book by James Rollins, victims of an unknown plague suffer from Prader-Willi as a side-effect, gorging themselves on human flesh until their stomachs explode."

Is this sentence relevant or necessary to an encyclopedic article about a congenital medical disorder? Does it augment the general understanding of the disease this article hopes to establish, or is it simply a plug for some fantasy novel? Inoculatedcities (talk) 00:35, 18 October 2011 (UTC)
 * I reworded it. The disorder is named in the book so I guess the item is as valid as any other 'in popular culture' reference.  I don't think it's a plug, but I think the person who added it may not have read the article carefully.  Saying victims "suffer from Prader-Willi as a side-effect" suggests the person who added it thinks that Prader-Willi syndrome is just another word for 'overating' rather than a disorder which causes overeating, among other things.  Also, viruses don't have 'side effects', they have symptoms.  Drugs and treatments have side effects. 68.33.14.232 (talk) 17:13, 28 November 2011 (UTC)

Published Clinical Diagnostic Criteria for PWS - 1993
Source: http://pediatrics.aappublications.org/content/108/5/e92.full.pdf

The purpose of scoring is to refer the subject for Genetic Testing.

To score, major criteria are weighted at 1 point each, and minor criteria are weighted at 1⁄2 point each. Supportive findings increase the certainty of diagnosis but are not scored. For children 3 years of age or younger, 5 points are required, 4 of which should come from the major group. For children 3 years of age and for adults, a total score of 8 is required and major criteria must comprise 5 or more points of the total score.

TABLE 1. Published Diagnostic Criteria for PWS Major Criteria 1. Neonatal and infantile central hypotonia with poor suck, gradually improving with age 2. Feeding problems in infancy with need for special feeding techniques and poor weight gain/failure to thrive 3. Excessive or rapid weight gain on weight-for-length chart (excessive is defined as crossing two centile channels) after 12 months but before 6 years of age; central obesity in the absence of intervention 4. Characteristic facial features with dolichocephaly in infancy, narrow face or bifrontal diameter, almond-shaped eyes, small- appearing mouth with thin upper lip, down-turned corners of the mouth (3 or more are required). 5. Hypogonadism — with any of the following, depending on age: a. Genital hypoplasia, (male: scrotal hypoplasia, cryptorchidism, small penis and/or testes for age ( 5th percentile); female: absence or severe hypoplasia or labia minora and/or clitoris b. Delayed or incomplete gonadal maturation with delayed pubertal signs in the absence of intervention after 16 years of age (male: small gonads, decreased facial and body hair, lack of voice change; female: amenorrhea/oligomenorrhea after age 16) 6. Global developmental delay in a child 6 years of age; mild to moderate mental retardation or learning problems in older children 7. Hyperphagia/food foraging/obsession with food 8. Deletion 15q11 – 13 on high resolution ( 650 bands) or other cytogenetic molecular abnormality of the Prader-Willi chromosome region, including maternal disomy Minor Criteria 1. Decreased fetal movement or infantile lethargy or weak cry in infancy, improving with age 2. Characteristic behavior problems – temper tantrums, violent outbursts, and obsessive-compulsive behavior; tendency to be argumentative, oppositional, rigid, manipulative possessive, and stubborn; perseverating, stealing, and lying (5 or more of these symptoms required) 3. Sleep disturbance and sleep apnea 4. Short stature for genetic background by age 15 (in the absence of growth hormone intervention) 5. Hypopigmentation — fair skin and hair compared with family 6. Small hands ( 25th percentile) and/or feet ( 10th percentile) for height age. 7. Narrow hands with straight ulnar borders 8. Eye abnormalities (esotropia, myopia) 9. Thick viscous saliva with crusting at corners of the mouth 10. Speech articulation defects 11. Skin-picking Supportive Findings 1. High pain threshold 2. Decreased vomiting 3. Temperature instability in infancy or altered temperature sensitivity in older children and adults 4. Scoliosis and/or kyphosis 5. Early adrenarche 6. Osteoporosis 7. Unusual skill with jigsaw puzzles 8. Normal neuromuscular studies

The article concludes: When definitive diagnostic testing is not available, as was the case for PWS when the 1993 criteria were developed, diagnostic criteria are important to avoid overdiagnosis and to ensure that diagnostic test development is performed on appropriate samples.

When diagnostic testing is available, as is now the case for PWS, diagnostic criteria should serve to raise diagnostic suspicion, ensure that all appropriate people are tested, and avoid the expense of testing unnecessarily. Results indicate that the sensitivities of most of the published criteria are acceptable. However, 16.7% of patients with molecular diagnosis did not meet the 1993 clinical diagnostic criteria retrospectively, suggesting that the published criteria may be too exclusive.

Photo (again) - caption and description say the opposite
The box with the photo says "Prader-Willi syndrome phenotype at 15 years of age. Note presence of typical PWS facial features and mild truncal obesity", while the image description page has "Note absence of typical PWS facial features and presence of mild truncal obesity". Which is considered correct? 212.225.122.45 (talk) 17:40, 30 October 2013 (UTC)
 * I've changed the description in the box on the page, as the source on PubMed explicitly matches that found on the page description. Even if some of the facial features seem present, I don't think we can reinterpret what the source says. 212.225.122.45 (talk) 17:46, 30 October 2013 (UTC)

Fairness of the name
So Labhart, Ziegler and Fanconi miss out? Shouldn't it be Prader-Willi-Labhart-Ziegler-Fanconi, or PWLZF? Just doesn't seem fair to the other cofounders? 134.148.71.167 (talk) 09:43, 8 October 2014 (UTC)

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Sourcing
I noticed that the 400,000 sufferer figure leads to a dead link on the Huffington Post website. I found the original source and it led me to another source, a 2002 paper:

Carrel AL, Myers SE, Whitman BY, Allen DB (April 2002). "Benefits of long-term GH therapy in Prader-Willi syndrome: a 4-year study". J. Clin. Endocrinol. Metab. 87 (4): 1581–5.doi:10.1210/jc.87.4.1581. .

I don't know how to properly modify the text for the sourcing on Wikipedia, so if anyone can do that change, that would be great. --Agamemnus (talk) 22:42, 17 October 2015 (UTC)

Appetite
The article's current description of the constant ravenous hunger which torments Prader-Willi patients seems understated, dry, and clinical. I don't wish to sensationalize, but as it stands, I fear that the reader may not get a true picture of how god-awful this syndrome is, for the patients, and for the care-givers, who must relentlessly steel themselves against the patients' unceasing, and often heart-rending, demands for more food. I am attempting to correct this, and I am mentioning the fact that caregivers need to strictly limit access to food, usually by installing locks on the refrigerator and on all food-storage places. With a reference, of course. HandsomeMrToad (talk) 10:12, 16 June 2016 (UTC)
 * Nothing wrong with dry. Doc James  (talk · contribs · email) 16:23, 4 September 2016 (UTC)

PWS is not autosomal dominant, it is a genetically imprinted syndrome
PWS is not an autosomal dominant disorder and this is a huge miscommunication. PWS is a genetically imprinted syndrome (the first one ever identified if I am not mistaken). Normally healthy adults have expression of both maternal and paternal PWS critical region genes on chromosome 15q11.2-13. About 3/4 of PWS patients have absence of paternally derived genes here, the remainder are due to various rare or yet to be elucidated mechanisms. The maternally inherited genes are silent in all normal people, with loss of the paternal genes due to imprinting PWS ensues. It is misleading to call this an autosomal dominant disorder, if that terminology is used it should be explained in further detail. It is generally believed that the imprinting is caused by methylation of the allele, not an autosomal dominant phenomenon. Source: $500k medical education, Robbins & Cotran 9e.
 * Thanks. We have another good ref  Doc James  (talk · contribs · email) 02:01, 10 April 2017 (UTC)

Harvey Price
Put Harvey price in. Sky living documentary/ evening standard/ any number of guff tabloid nonsense you have a channel 4 documentary as a behaviour Source. I fail to see how Harvey is getting excluded. Racism? — Preceding unsigned comment added by 86.139.68.14 (talk) 21:45, 12 April 2017 (UTC)

 * Could you provide one good source here? But even if you could, there is currently no section for "Notable cases" in this article, so the addition of one celebrity name would be wholly unbalanced and contrary to WP:WEIGHT. Thanks. Martinevans123 (talk) 22:33, 12 April 2017 (UTC)

http://www.radiotimes.com/blog/2011-07-01/tv-ratings-320000-watch-katie-prices-harvey-documentary-on-sky-living please see original documentary. Discussed at some length are there many other people with the condition in the public eye?
 * Source does not even say Prader Doc James  (talk · contribs · email) 03:03, 13 April 2017 (UTC ill)

Fair do's the doc does talk about it at length, but we can give Harvey a by if you want to patch it. Can I slam in some info from a study on pws mouse models? Have some interesting info on negative feedback loops and malformation of enzymes/changes in activation energonics.

 * No, you can't. Martinevans123 (talk) 20:13, 13 April 2017 (UTC)

Awfully silly.

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This is a disease caused by A loss of function in a genetic gene, specifically in chromosome number 15 (is deleted).That could cause various disabilities, some of these disabilities are behavior problems, intellectual disability, and short stature. 161.45.254.242 (talk) 12:47, 1 October 2018 (UTC)

Prader- Willi syndrome
PWS is not inher ited but instead the genetic changes happen during the formation of the egg, sperm, or in early development.[3] There has not been any risk factors due to this inheritance.[7] Those who have one child with PWS have less than a 1% chance of the next child being affected.[7] syndrome (PWS) is a genetic disorder caused by the loss of function of specific genes.[3] In newborns symptoms include weak muscles, poor feeding, and slow development.Martinafarag (talk) 14:59, 3 October 2018 (UTC)

 * Do you have a particular point to make here, or do you have a question? Thanks. Martinevans123 (talk) 22:41, 16 November 2018 (UTC)

Prader- Willi syndrome
The treatment, however, may improve outcomes, especially if carried out early.[4] In newborns feeding difficulties may be supported with feeding tubes.[6] Strict food supervision is typically required starting around the age of three in combination with an exercise program.[6] Growth hormone therapy also improves outcomes.[6] Counseling and medications may help with some behavioral problems.[6] Group homes are often necessary in adulthoodFatema alkhafaji (talk) 15:02, 3 October 2018 (UTC)

Genetics: “During the early 1980s, scientists puzzled over why some people who seemed to have PWS did not have the chromosome 15 deletion, and why some people with the chromosome 15 deletion seemed to have a different condition from PWS. Dr. Merlin Butler and colleagues began unraveling the puzzle when they reported in 1983 that the chromosome 15 deletion in PWS was on the father’s chromosome” (pwsausa.org). In other words, PWS is not only just caused by deletion of chromosome 15 but can also be caused by maternal uniparental and imprinting defect (pwsausa.org). The other type of PWS is an individual person have duplicated chromosomes (ghr.nlm.nih.gov). “PWS in conjunction with Angelman syndrome (AS) represent perhaps the best examples of genomic imprinting in humans. The majority of the genes in mammals display a Mendelian pattern of expression where normal alleles inherited from each parent are equally expressed” (nature.com). Which means that the parental code or gene is being deleted from the offspring also deleting the same chromosome from the maternal side causing Angelman syndrome disease. “The exact function of each of the genes in determining the PWS phenotype remains to be elucidated, although possible insight has been gained by work with mouse models by multiple investigators” (nature.com). After all the work scientists have done, there is still not a specific reason why PWS would happen. “Furthermore, rigorous neurobehavioral studies have not been performed to determine whether these individuals have the typical PWS behavioral phenotype” (nature.com). Even though, there has been a lot of advances in understanding the genetic changes associated with the diseases of PWS; however, the symptoms and genetics region associated with that disease is not understood (fpwr.org). The PWS occurred “In a very small proportion of affected people, PWS has occurred due to a balanced translocation of chromosome 15” (rarediseases.org). PWS can also be caused by the rearrangement of chromosomes, also known as translocation (ghr.nlm.nih.gov). Furthermore, PWS genes are put into four different regions based on common deletion: a proximal non-imprinted, the PWS paternal-only expressed region, the Angelman syndrome (AS) region, and a distal non imprinted region (nature.com). Scientists also believe that there might be other chromosomes that causes PWS. Moreover, there might be some chromosome that works with chromosomes 15 to cause PWS (ghr.nlm.nih.gov). For example, a symptom for PWS is light hair color, the chromosome that is responsible for hair color is OCA2, which is part of chromosome 15 (ghr.nlm.nih.gov). Which means that if chromosome 15 is deleted, OCA2 will get affected, leading to more genetic issues. Such as the human’s phenotype (ghr.nlm.nih.gov).Maryelkommos (talk) 17:21, 16 November 2018 (UTC)Maryelkommos (talk) 16:54, 19 November 2018 (UTC) [http://www.nature.com/articles/gim0b013e31822bead0. www.nature.com/articles/gim0b013e31822bead0. ] [http://www.fpwr.org/about-prader-willi-syndrome#hereditary. www.fpwr.org/about-prader-willi-syndrome#hereditary. ] [http://www.pwsausa.org/genetics-of-pws/. www.pwsausa.org/genetics-of-pws/. ]https://ghr.nlm.nih.gov/condition/prader-willi-syndrome https://ghr.nlm.nih.gov/condition/prader-willi-syndrome https://rarediseases.org/rare-diseases/prader-willi-syndrome/ Maryelkommos (talk) 17:35, 19 November 2018 (UTC)

Treatment and Management:

The most effective and efficient mode of PWS treatment is through adopting a multi-disciplinary approach. The multidisciplinary action comprises early disease diagnostics, early interdisciplinary action on therapy as well as the treatment growth hormone. For instance, PWS management is dependent on the patient’s age and related symptoms. Following PWS diagnosis, evaluations are made to diagnose the extents of the condition. This diagnosis is further based on age. Newborns are assessed on the basis of sucking challenges. Infants are assessed on the grounds of growth development and young children are diagnosed on the basis of a vision exam. On the other hand, all male patients are evaluated for the presence or absence of cryptorchidism. For treatment or management, infants are introduced to specialize feeding techniques immediately after definite diagnosis (Driscoll Schwartz and Cassidy, 2016). Additionally, young children suffering from PWS also need immediate intervention concerning physical therapy. This therapy is aimed at developing an enhancing muscle strength enabling them to reach physical milestones. The early intervention also involves speech therapy needed to solve language issues. Cryptorchidism, on the other hand, may be left to phase out naturally but in most cases requires hormonal treatment. In instances of young children approaching obese, affected children should be scheduled for balanced diet programs, exercise sessions as well as food uptake scrutiny. In such cases, there is a need for consultation with professional dietitians (Butler, Dykens, and Gold et al. 2018). Abnormal behavioral patterns, on the other hand, may be addressed by employing special behavioral management programs. For adults with obsessive symptoms, injection of serotonin uptake inhibitors is helpful. Stature development can, on the other hand, be rectified by the uptake of growth hormone treatments in the form of growth hormones. Growth therapies employed from infancy to adulthood impacts elements such as language and cognitive abilities as well as motor capabilities. Treatment and Management:

The most effective and efficient mode of PWS treatment is through adopting a multi-disciplinary approach. The multidisciplinary action comprises early disease diagnostics, early interdisciplinary action on therapy as well as the treatment growth hormone. For instance, PWS management is dependent on the patient’s age and related symptoms. Following PWS diagnosis, evaluations are made to diagnose the extents of the condition. This diagnosis is further based on age. Newborns are assessed on the basis of sucking challenges. Infants are assessed on the grounds of growth development and young children are diagnosed on the basis of a vision exam. On the other hand, all male patients are evaluated for the presence or absence of cryptorchidism. For treatment or management, infants are introduced to specialize feeding techniques immediately after definite diagnosis (Driscoll Schwartz and Cassidy, 2016). Additionally, young children suffering from PWS also need immediate intervention concerning physical therapy. This therapy is aimed at developing an enhancing muscle strength enabling them to reach physical milestones. The early intervention also involves speech therapy needed to solve language issues. Cryptorchidism, on the other hand, may be left to phase out naturally but in most cases requires hormonal treatment. In instances of young children approaching obese, affected children should be scheduled for balanced diet programs, exercise sessions as well as food uptake scrutiny. In such cases, there is a need for consultation with professional dietitians (Butler, Dykens, and Gold et al. 2018). Abnormal behavioral patterns, on the other hand, may be addressed by employing special behavioral management programs. For adults with obsessive symptoms, injection of serotonin uptake inhibitors is helpful. Stature development can, on the other hand, be rectified by the uptake of growth hormone treatments in the form of growth hormones. Growth therapies employed from infancy to adulthood impacts elements such as language and cognitive abilities as well as motor capabilities.Sandyyossef (talk) 18:57, 16 November 2018 (UTC) Diagnosis and Testing: In establishing the presence or absence of PWS in patients’ health professionals have employed a concept referred to as DNA methylation testing. This technique is aimed at detecting an abnormality in parent-oriented imprinting of genes in the chromosome 15 areas that is responsible for the disease. It also further establishes whether the anomaly is maternal or paternal only (Gunay- Schwartz and Heeger, 2001). This technique is mostly applicable in infants or patients who are too young to exhibit enough signs and symptoms to make an informed diagnosis. Information regarding the PWS testing available in the Genetic Testing Registry is open to healthcare professionals. Therefore, information regarding the PWS testing can only be obtained by consulting the healthcare provider (Holm, Hanchett and Whitman et al., 1993).Sandyyossef (talk) 18:57, 16 November 2018 (UTC) Sandyyossef (talk) 18:57, 16 November 2018 (UTC)

Diagnosis and Testing:

Prader–Willi syndrome (PWS) is a multi-systemic complex genetic disorder caused by lack of expression of genes in chromosome 15q11.2-q13 region that are inherited paternally (Driscoll, 2017). PWS results in disruption of functions of hypothalamus affecting sexual development, growth, body temperature, mood, sleep and response to hunger (Rodriguez, 2018). There are three genetic subtypes of PWS i.e. paternal deletion of 15q11.2-q13, maternal uniparental disomy and imprinting defect. Diagnosis of PWS is made by the physician using clinical symptoms. There should be early diagnosis in infants since hypotonia which refers to condition of muscle weakness is evident (Bar, 2017). The diagnosis is made through blood tests and the most preferred method of diagnosis is DNA methylation analysis which detects all genetic subtypes of PWS and differentiates it from Angelman syndrome (Robertson, 2005). In infants, the signs and symptoms are; Primary sign is hypotonia which is poor muscle tone that results in poor sucking reflex (Angulo, 2015). The elbows and knees are loosely extended rather than fixed. There is lethargy characterized by poor response to stimuli and fatigue, the infant also has distinct facial features that are not normal and may have underdeveloped genitals i.e. small penis and scrotum in males and small labia and clitoris in females (Driscoll, 2017). Other signs appear at early childhood and are exhibited until adulthood and these symptoms require careful management (Bar, 2017). Hyperphagia that starts at two years and continues to adulthood makes the patient overfeed leading to complications of obesity and obsessive behavior towards food. The patient has hypogonadism resulting in sexual organs underdevelopment due to production of no or little sex hormones in testes and ovaries. There is Poor growth and physical development due to underproduction of growth hormones, hypothyroidism which causes poor management of stress. There are sleep disorders, behavioral and speech problems (Angulo, 2015). Cognitive impairment that causes poor thinking and reasoning, a child with PWS also experiences delay in motor development than other normal children. Other signs may include scoliosis which is curvature of spine and also hypopigmentation causing hair, skin and eyes to become pale. These symptoms may lead to diagnosis of PWS but does not rule out Angelman Syndrome since they share same symptoms (Driscoll, 2015). Differential diagnosis is done through methylation analysis. DNA methylation analysis presents a definitive test for PWS (Robertson, 2005). Normal individuals have both methylated and unmethylated allele from both parents while individuals with PWS have only maternally methylated allele and thus DNA methylation provide efficient diagnosis of PWS and rules out Angelman syndrome which contains paternal methylated allele (Robertson, 2005). This method exploits 5′ CpG Island of the SNRPN locus diagnosing 99% of the cases (Driscoll, 2017). However, this method does not define the type of PWS and thus methylation-specific multiplex-ligation probe amplification (MS-MLPA) is used to differentiate the three subgroups. MS-MLPA will determine methylation status that lead to identification of typical deletion. High-resolution microarrays help in identifying maternal disomy or imprinting defect (Robertson, 2005).Fatema alkhafaji (talk) 02:13, 18 November 2018 (UTC)(UTC)https://www.ncbi.nlm.nih.gov/sites/books/NBK1330/.https://www.ncbi.nlm.nih.gov/pubmed/16136652.https://www.jci.org/articles/view/99725.https://ojrd.biomedcentral.com/articles/10.1186/s13023-017-0673-6.https://www.ncbi.nlm.nih.gov/pubmed/26062517.

Epidemiology and Society and Culture:

The Prader-Willi Syndrome (PWS) can occur and does occur in both male and female babies. It is a very rare disease, with chances of newborn’s born with the illness varying between 1 in 10,000 and 1 in 25,000 (Killeen 2004). Although it is very rare, it is still the most common form of an obesity illness there is (Scheimann 2017). There are currently over 400,000 people who have PWS and both sexes are equally likely to develop the syndrome (Scheimann 2017). According to the Prader Willi Syndrome Association, an average of 65 percent of people are not aware that they have the illness (PSWA). According to the 2010 Census, there was a total of over 308 million people living in the United States. From those people, 7,206 of them had PWS. The amount of people that had the illness in 2010 in the United States was a lot less than 1 percent. This only proves how rare it is. The United States and the United Kingdom have a larger population of people with PWS than the rest of the countries in the world (Scheimann 2017). Our Society shows us how serious Prader Willi Syndrome is but also in some ways take it not so seriously. On the positive side, there was a multi episode documentary like showing of a series in the United Kingdom in 2007. The documentary was based on a plot of two people who lived with PW syndrome. The show was titled “Can’t Stop Eating” (K12 Academics). The title of this show is deep in a way not anyone will understand. When people first here of PWS, they usually only think of the exterior physical effects of the illness. Like chunkiness, rolls, width, and obvious abnormal weight. People around them don’t usually think about how it affects them internally. Along with the exterior affect, comes an internal desire for food constantly, hence the name “Can’t Stop Eating”. The phrase emphasizes on how people with the syndrome are affected against their will. They can not control their desire for food, as if they never feel full or eat in situations where others aren’t. The negative side of society looks at these people and judges them calling them fat and disgusting, with no sympathy for the possibility that they may have an illness. So many illnesses and diseases exist that others are not familiar with. This genetic disease is extremely rare but can tremendously impact lives. What most people don’t know is that people with PWS find difficulty in everything they do more than others around them who don’t have the syndrome. They have a hard time with speech, learning, physical activity, eating habits, sleeping, socializing, and other fairly important factors. People with PWS, especially the ones attending school, may very likely need extra special attention and should be in a smaller classroom where the teacher is able to give them enough attention (NIH 2015). Most of them also need a way of keeping them away from overeating, whether they like to or not. It is not under their control and should get help (NIH 2015). The patient with PWS, along with their loved ones, are affected daily by the disorder, whether directly or indirectly. The Genetics Education Materials for School Success (GEMSS), is a program that offers help and information about how a child with PWS can be or is already helped in school. This program can help assure parents and help teachers better understand what a child with PWS may need (NIH 2015). There are three official organizations that are able to help a family with a loved one who suffers from PWS: Foundation for Prader-Willi Research, International Prader-Willi Syndrome Organisation (IPWSO), and the Prader-Willi Syndrome Association.

https://www.k12academics.com/disorders-disabilities/prader%E2%80%93willi-syndrome/society-culture. https://www.uptodate.com/contents/epidemiology-and-genetics-of-prader-willi-syndrome. https://www.pwsausa.org/pws-statistics/. https://rarediseases.info.nih.gov/diseases/5575/prader-willi-syndrome. https://www.gemssforschools.org/about/default. Josephinedemian (talk) 05:37, 18 November 2018 (UTC)Josephine Demian

 * Hi Josephinedemian. This Talk page is meant for discussing improvements to the article. I wonder are you proposing that the above text is included in the article? It seems that you may have copied and pasted most of that material from the sources linked? Thanks. Martinevans123 (talk) 09:41, 18 November 2018 (UTC)
 * This class has run into some major misunderstandings when it comes to what they are supposed to be doing on Wikipedia. It's probably better than they posted this to the talk page, rather than the article space. Ian (Wiki Ed) (talk) 19:39, 19 November 2018 (UTC)
 * Haha, yes. I think we can all agree with that! Do you think it's a good idea to keep it all here?? Thanks. Martinevans123 (talk) 19:43, 19 November 2018 (UTC)
 * If it's OK, I'd prefer to leave it until the semester is done. Ian (Wiki Ed) (talk) 00:02, 20 November 2018 (UTC)
 * Ian (Wiki Ed), I really don't think it's a matter of your preference, or indeed mine. I wonder could you explain how this material comes to be here? Ismn't this the sort of draft work that is supposed to reside in the respective editors' sandboxes? Is there expected to be an eventual benefit to the article from all this and, if so, when? Would it be possible to hat all of this material so that it is less distracting for normal editors? Many thanks for your consideration. Martinevans123 (talk) 16:52, 20 November 2018 (UTC)
 * I wish I could explain how it happened. Despite having the same guidance and training modules as hundreds of other classes we've supported, this class ended up producing content that was clearly unsuitable for mainspace. It's especially unfortunate because they produced a lot of content - had their efforts been in the right direction, they could have created a lot of good content. The group working on this article seem to have decided that they should be posting here. A few individuals always go wrong, but I'm especially bothered by the fact that almost a whole class did.
 * As for the content - yes, of course you should feel free to hat it. I can always track it down for the instructor if they're trying to find work to grade. Once the term is done though, it's probably best to archive or delete it (which I'd be happy to do). Ian (Wiki Ed) (talk) 17:20, 20 November 2018 (UTC)
 * Many thanks. Sounds like a good plan. Martinevans123 (talk) 17:29, 20 November 2018 (UTC)

Signs and Symptoms

Depending on the individual signs and symptoms of Prader- Willi syndrome will vary. As humans grow these symptoms may change from childhood to adulthood. Symptoms that may occur in infants happen during birth. These symptoms include poor muscle tone, distinct facial features, poor sucking reflex, generally poor responsiveness, and underdeveloped genitals. For early childhood to adulthood these symptoms usually appear during early childhood and remain throughout life. These symptoms are food craving and weight gain, underdeveloped sex organs, poor growth and physical development, cognitive impairment, delayed motor development, speech problems, and sleep disorders. Prader- Willi syndrome in infants is caused by weak muscle tone, feeding defects, poor growth, and delayed development. This leads children who are affected to overeat. Some ways you can tell if your baby has Prader-Willi syndrome is if they have almond-shaped eyes which is due to the lack of muscle tone, their head will get narrow at the temples, their mouth might turn down at the corners, and having a thin upper lip. People with PWS don’t get full, which causes them to overeat because they never feel full. Signs of this is nonstop hunger and weight gain. Children with PWS will always want more food, they will try to hide food to eat it later, and some children will eat food that’s frozen or food out of the garbage. Children with PWS usually are short for their age, they have small hands and feet, they will have extra body fat and not enough muscle mass, they are usually slow in talking, sitting, standing or walking, they will have having learning problems, and having sleep problems. PWS develops in two stages, the first stage is between 0 and 12 months and the second stage are from age 1 to 6 years. Children between 0 and 12 months will have unusual weak cries, they will have a difficult time waking up, they will appear tired, their genitals may not develop correctly, and lastly, they will have depigmentation of the skin and sometimes their eyes. A mother can also tell if her baby will have PWS due to fetal movements in the belly as well as the abnormal fetal positions. For children at the age of 1 to 6 years will have high levels of pain and that is for phase 1. For phase 2 which is from 18 to 36 months, children’s body weight goes from lower than average to higher without food or calorie intake. In phase 3 it starts at the age of 8 years old and goes into adulthood. This age is when the intake of more food intake starts, children with PWS also undergo poor sexual development during puberty. If the child is a female with PWS may not get their menstrual cycled and adults with PWS may not be able to reproduce. Children with PWS have unusual cognitive profiles, they tend to have a strong vocabulary and they read very well. But when it comes to speaking they are usually poor in it. Children with PWS also have a hard time processing thing. These symptoms may improve as they grow to adulthood, but it’s not always guaranteed.Martinafarag (talk) 15:36, 19 November 2018 (UTC)https://www.mayoclinic.org/diseases-conditions/prader-willi-syndrome/symptoms-causes/syc-20355997. https://rarediseases.info.nih.gov/diseases/5575/prader-willi-syndrome.https://www.webmd.com/parenting/baby/prader-willi-syndrome#1.https://www.medicalnewstoday.com/articles/182287.php.https://www.medicinenet.com/prader-willi_syndrome/article.htm#how_common_is_and_what_causes_prader-willi_syndrome.

Genetics: “During the early 1980s, scientists puzzled over why some people who seemed to have PWS did not have the chromosome 15 deletion, and why some people with the chromosome 15 deletion seemed to have a different condition from PWS. Dr. Merlin Butler and colleagues began unraveling the puzzle when they reported in 1983 that the chromosome 15 deletion in PWS was on the father’s chromosome” (pwsausa.org). In other words, PWS is not only just caused by deletion of chromosome 15 but can also be caused by maternal uniparental and imprinting defect (pwsausa.org). The other type of PWS is an individual person have duplicated chromosomes (ghr.nlm.nih.gov). “PWS in conjunction with Angelman syndrome (AS) represent perhaps the best examples of genomic imprinting in humans. The majority of the genes in mammals display a Mendelian pattern of expression where normal alleles inherited from each parent are equally expressed” (nature.com). Which means that the parental code or gene is being deleted from the offspring also deleting the same chromosome from the maternal side causing Angelman syndrome disease. “The exact function of each of the genes in determining the PWS phenotype remains to be elucidated, although possible insight has been gained by work with mouse models by multiple investigators” (nature.com). After all the work scientists have done, there is still not a specific reason why PWS would happen. “Furthermore, rigorous neurobehavioral studies have not been performed to determine whether these individuals have the typical PWS behavioral phenotype” (nature.com). Even though, there has been a lot of advances in understanding the genetic changes associated with the diseases of PWS; however, the symptoms and genetics region associated with that disease is not understood (fpwr.org). The PWS occurred “In a very small proportion of affected people, PWS has occurred due to a balanced translocation of chromosome 15” (rarediseases.org). PWS can also be caused by the rearrangement of chromosomes, also known as translocation (ghr.nlm.nih.gov). Furthermore, PWS genes are put into four different regions based on common deletion: a proximal non-imprinted, the PWS paternal-only expressed region, the Angelman syndrome (AS) region, and a distal non imprinted region (nature.com). Scientists also believe that there might be other chromosomes that causes PWS. Moreover, there might be some chromosome that works with chromosomes 15 to cause PWS (ghr.nlm.nih.gov). For example, a symptom for PWS is light hair color, the chromosome that is responsible for hair color is OCA2, which is part of chromosome 15 (ghr.nlm.nih.gov). Which means that if chromosome 15 is deleted, OCA2 will get affected, leading to more genetic issues. Such as the human’s phenotype (ghr.nlm.nih.gov). Maryelkommos (talk) 17:36, 19 November 2018 (UTC) [http://www.nature.com/articles/gim0b013e31822bead0. www.nature.com/articles/gim0b013e31822bead0. ] [http://www.fpwr.org/about-prader-willi-syndrome#hereditary. www.fpwr.org/about-prader-willi-syndrome#hereditary. ] [http://www.pwsausa.org/genetics-of-pws/. www.pwsausa.org/genetics-of-pws/. ]https://ghr.nlm.nih.gov/condition/prader-willi-syndrome https://ghr.nlm.nih.gov/condition/prader-willi-syndrome https://rarediseases.org/rare-diseases/prader-willi-syndrome/Maryelkommos (talk) 17:37, 19 November 2018 (UTC)

Ketogenic diets for Prader-Willi
there are many Patients with Prader-Willi practicing (modified) ketogenic-diets, who report improved quality of life, improved cognition and reduced appetite. mostly this is reported via blogs and social networks (I was explained that such links don't fit wikipedia) there exists an 1970 study, which summarizes that ketogenic diet for Prader-Willi results with decreased appetite - here : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4955809/ there exists an 2017 study, which summarizes that modified ketogenic diet for Prader-Willi results with many areas of improved life quality - here : https://www.pws.org.nz/wp-content/uploads/2018/06/TREND-Community-Diet-Initiative-Overview.pdf

is there a way to incorporate this information in the prader-willi page ?

MulaLiron (talk) 14:37, 14 December 2018 (UTC)

praders willi
Someone in my class has it and we yeah bye :) — Preceding unsigned comment added by 47.154.8.115 (talk) 02:54, 30 May 2019 (UTC)

Life expectancy?
The wiki article about a genetically similar but functionally different syndrome, Angleman syndrome indicates that life expectancy for that condition is normal; could someone find/add that info for this condition to this article? UnderEducatedGeezer (talk) 12:46, 16 September 2019 (UTC)

Title formatting
The current title uses an en dash between Prader and Willi. The article was originally created with a hyphen, but was moved with WP:MOS as the justification. But the relevant section of the MOS states: "Generally, use a hyphen in compounded proper names of single entities", and gives the example of Wilkes-Barre, PA, which is named after two people. That's the same situation as here. (The en dash serves to show a separation between the two, as opposed to the hyphen linking them.) As such, I believe this article should be moved back to the hyphenated version, Prader-Willi syndrome. Thoughts? — tooki (talk) 01:01, 26 November 2019 (UTC)
 * Yes. There seem to be quite a few listed under Category:Rare syndromes which are similarly two-name origin and use a hyphen? Martinevans123 (talk) 11:08, 26 November 2019 (UTC)

Treatment
There is treatment for the condition, but the narrator in Mystery Diagnosis says there is isn't. — Preceding unsigned comment added by 2601:18D:4700:2D30:8DF5:587:8E9F:B861 (talk) 21:02, 25 December 2021 (UTC)

Life expectancy?
Reading through the article, there doesn't seem to be any mention as to whether or not P-WS has any effect on one's life expectancy.

In a local newspaper I noticed a woman with this condition died at age 34. I don't know if this is typical or not? StuZealand (talk) 11:50, 15 July 2023 (UTC)

No mention of Tarrare?
I read up that modern historians(?) believe he had this, so I came to the page to read up about it. But there's nothing about it. Not here, and not in Tarrare either. What's up with that? Could it have been fake news? I'm interested in knowing what are the cases for it, against it, other 'known' people that might've had PWS... this is a thing in other pages like this, is it not? 186.212.9.15 (talk) 21:33, 10 July 2024 (UTC)

title: Talk:Prader–Willi syndrome


text:
Lionheart: Legacy of the Crusader

Lionheart: Legacy of the Crusader is an action role-playing game developed by Reflexive Entertainment and published by Interplay Entertainment subsidiary Black Isle Studios for Windows, released in August 2003. The game is viewed from a 3/4 isometric camera angle. It focuses on a protagonist, controlled by the player, as he travels on a quest that constitutes the central focus of the game. The plot stipulates a rift in reality that drastically altered medieval history by allowing demons and other similar beings to enter the mortal realm. During the game, the protagonist encounters and interacts with numerous historical figures such as Joan of Arc, Leonardo da Vinci and Galileo Galilei who are represented as non-player characters.

Lionheart utilizes the SPECIAL role-playing system, which was first used in the Fallout series, and in this game functions primarily in adding points to specific skills in separate trees to strengthen a character's "Spiritkind", which has a personality and nature chosen by the player at the start of the game.

Gameplay
As Lionheart implements the SPECIAL system, the character creation is similar to that of the Fallout series. Players begin by setting the values of their characters' strength, perception, endurance, charisma, intelligence, agility and luck, and selecting "traits", which alter a character's inherent abilities for either better or worse, for the duration of the game. In addition, the player must distribute points to "skills" – abilities which a character uses to achieve various effects. One skill, "diplomacy," allows the player to talk their way out of situations gone awry, while another, "sneak", allows the player to move undetected by enemies. Unlike the Fallout series, Lionheart also allows the player to select magical skills – an example being "discord", which turns hostile enemies against one another.

Players also select "perks" during the course of the game – abilities similar to traits, which affect a character's abilities in some form. For example, the ability "Superior Senses" grants the player character a +1 bonus to his or her perception and +15 skill points in the "find traps/secret doors" skill.

Another element newly introduced by Lionheart is the player's selection of a "Spiritkind" for their character, which is done during character generation at the game's start. A Spiritkind is a spirit, which is either demonic, elemental or bestial, that resides in the player character and occasionally rouses to explain happenings or gameplay mechanics, or advance the plot.

The character generated by the player is the only character a player has direct control over, and though characters will occasionally join a player's adventuring party, they are AI-controlled without exception.

Plot
The setting of Lionheart is an alternate history created by the occurrence of the Disjunction, a rip in the fabric of time that introduces magic into the world. This event occurred when Richard the Lionheart massacred prisoners at the Siege of Acre during the Third Crusade, a decision exploited by a mysterious source to fuel a ritual that tore the fabric of reality and caused magic to enter the world from other dimensions.

The game takes place in 1588 and initially set in an alternate history version of Barcelona. In this time, the Spanish Armada is almost set to invade England, and the Inquisition is rampant. Lionheart features several Renaissance figures who make ahistorical appearances in the game, including Miguel de Cervantes, William Shakespeare, Galileo Galilei, Niccolò Machiavelli, and Leonardo da Vinci.

The plot of Lionheart sees the player character, discovered to be a descendent of Richard the Lionheart, inherit the powers obtained during the Disjunction. Players follow the story through aligning with one of the four main factions in the game – the Knights Templar, the Inquisition, the Knights of Saladin and the Wielders – and are tasked with stopping an attempt to permanently open the dimensional rift, and alter the course of European history.

Development
Reflexive Entertainment was approached by Black Isle Studios to develop a game after playing their previous title Zax: The Alien Hunter, an isometric game using the same engine. Ion Hardie states Black Isle originally wanted Reflexive Entertainment to develop a game in the vein of Fallout using the SPECIAL system. Chris Avellone recalls the decision to use SPECIAL was an attempt to "try and help boost sales by leveraging Fallout fan interest".

Production of Lionheart was strained, with both developer and publisher in financial stress. Ion Hardie notes Reflexive Entertainment was "literally one day away from making hard choices that might have shut us down for good when we got the contract (for Lionheart)". Interplay also bore significant financial issues that prevented them from providing the developer with milestone payments, with Hardie stating "(Interplay) had issues getting us the initial payment.

Release
Lionheart went gold on 16 July 2003. As with other Interplay titles at the time, Vivendi Universal Games handled North American distribution while Avalon Interactive handled European distribution. The game was released in 2003 in North America on 12 August, Australia on 26 August, and the United Kingdom on 12 September.

Reception
Lionheart received "mixed" reviews according to the review aggregation website Metacritic. GameSpot's Greg Kasavin noted that although Lionheart seems to promote diverse character creation, the significant focus on monster-infested areas "all but forces you to play as some sort of combat-oriented character." The game was also criticised for its attempts at promoting "Diablo-style," hack-and-slash gameplay after a more dialogue-driven approach in the earlier stages of the game. IGN's Barry Brenesal wrote, "the problem of deciding what kind of game it really wants to be, RPG or Diablo clone, is probably the most serious problem it's got." He continued that Lionheart "feels like a good game got lost somewhere en route, and ended up being pushed out the door with some basic features missing." RPGamer's Steven Bellotti assessed that the game "starts out so promising," but "once you get out of Barcelona and into the wider world, [it] falls flat on its face."

Conversely the game was praised for both its musical score, which was described as "excellent," and voice-acting, which was exclaimed to be "top-notch." The SPECIAL system-fueled character creation was called "great."

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

title: Lionheart: Legacy of the Crusader


text: User talk:68.85.253.247

title: User talk:68.85.253.247


text:
United States v. Ballard

United States v. Ballard, 322 U.S. 78 (1944), was a United States Supreme Court case from the October 1943 term.

The case arose from the appeal of the conviction of two leaders of the new religious "I AM" Activity movement for fraudulently seeking and collecting donations on the basis of religious claims that the defendants themselves did not believe.

The Supreme Court held that the question of whether the defendants' claims about their religious experiences were actually true should not have been submitted to a jury. The Court arrived at this conclusion in part because the "freedom of religious belief... embraces the right to maintain theories of life and of death and of the hereafter which are rank heresy to followers of the orthodox faiths." However, the Court did not address the issue of whether the sincerity of the defendants' beliefs was a proper question for the jury.

Justice Robert H. Jackson, dissenting, would have gone even farther, suggesting that the entire case should be dismissed for coming too close to being an investigation into the truth of a religious conviction. He would have held unconstitutional a jury determination of whether the defendants' religious beliefs were sincere, as well as whether they were true.

Prior history
After Guy Ballard's death, his wife, Edna Anne Wheeler Ballard, and son, Donald Ballard, were indicted for 18 counts of fraud. The indictment charged that the Ballards fraudulently collected over $3 million from their followers on the basis of religious claims the Ballards knew were false. Their followers protested outside the courthouse.

The District Court instructed the jury to convict if they found that the Ballards did not have a good faith belief in their religious claims. The Ballards were convicted.

The United States Court of Appeals for the Ninth Circuit overturned the conviction and granted a new trial, declaring that the District Court erred in restricting the issue to whether the defendants had a good faith belief in their claims. The government appealed to the Supreme Court.

Majority opinion

 * Written by : William O. Douglas; joined by : Black, Reed, Murphy, Rutledge

The majority opinion reversed the decision of the Court of Appeals and remanded the case to that court, ruling that the question of the truth or falsity of the beliefs had been rightly withheld from the jury. There was no ruling on the propriety of the jury instructions regarding the sincerity of the defendants' beliefs. In his majority opinion, Justice Douglas wrote: "The religious views espoused by respondents might seem incredible, if not preposterous, to most people. But if those doctrines are subject to trial before a jury charged with finding their truth or falsity, then the same can be done with the religious beliefs of any sect. When the triers of fact undertake that task, they enter a forbidden domain. The First Amendment does not select any one group or any one type of religion for preferred treatment. It puts them all in that position."

Chief Justice Stone's dissent

 * Written by : Stone; joined by : Roberts, Frankfurter

Chief Justice Stone, dissenting, argued that the question of truthfulness was appropriate for the jury: "I am not prepared to say that the constitutional guarantee of freedom of religion affords immunity from criminal prosecution for the fraudulent procurement of money by false statements as to one's religious experiences, more than it renders polygamy or libel immune from criminal prosecution... I cannot say that freedom of thought and worship includes freedom to procure money by making knowingly false statements about one's religious experiences."

Justice Jackson's dissent
Justice Jackson dissented because he believed that the First Amendment foreclosed inquiry into both the truthfulness of the defendants' religious claims and their sincerity. He would have dismissed the case entirely for being too close to a religious persecution: "I should say the defendants have done just that for which they are indicted. If I might agree to their conviction without creating a precedent, I cheerfully would do so. I can see in their teachings nothing but humbug, untainted by any trace of truth. But that does not dispose of the constitutional question whether misrepresentation of religious experience or belief is prosecutable; it rather emphasizes the danger of such prosecutions."

"Prosecutions of this character easily could degenerate into religious persecution." "I would dismiss the indictment and have done with this business of judicially examining other people's faiths." "All schools of religious thought make enormous assumptions, generally on the basis of revelations authenticated by some sign or miracle." "Some who profess belief in the Bible read literally what others read as allegory or metaphor, as they read Aesop's fables." "If we try religious sincerity severed from religious verity, we isolate the dispute from the very considerations which, in common experience, provide its most reliable answer." "William James, who wrote on these matters as a scientist, reminds us that it is not theology and ceremonies which keep religion going. Its vitality is in the religious experiences of many people. 'If you ask what these experiences are, they are conversations with the unseen, voices and visions, responses to prayer, changes of heart, deliverances from fear, inflowings of help, assurances of support, whenever certain persons set their own internal attitude in certain appropriate ways.'" "If religious liberty includes, as it must, the right to communicate such experiences to others, it seems to me an impossible task for juries to separate fancied ones from real ones, dreams from happenings, and hallucinations from true clairvoyance. Such experiences, like some tones and colors, have existence for one, but none at all for another. They cannot be verified to the minds of those whose field of consciousness does not include religious insight. When one comes to trial which turns on any aspect of religious belief or representation, unbelievers among his judges are likely not to understand, and are almost certain not to believe, him."

Subsequent history
On remand to the United States Court of Appeals for the Ninth Circuit the original conviction was affirmed without rehearing by the Court of Appeals. The defendants once again petitioned for a writ of certiorari and it was once again granted, this time on the issue of women being excluded from grand jury and the trial jury. The Supreme Court ruled in favor of the defendants and dismissed the indictment as well as the subsequent conviction.

title: United States v. Ballard


text:
Kaz (cartoonist)

Kazimieras Gediminas Prapuolenis (born July 31, 1959), known professionally as Kaz, is an American cartoonist, animator, writer, storyboard artist, and illustrator. In the 1980s, after attending New York City's School of the Visual Arts, he was a frequent contributor to the comic anthologies RAW and Weirdo. Since 1992, he has drawn Underworld, an adult-themed syndicated comic strip that appears in many alternative weeklies.

Career
Kaz's comics and drawings have appeared in many alternative and mainstream publications including Details, The New Yorker, Nickelodeon Magazine, The Village Voice, East Village Eye, Swank, RAW, Eclipse, N.Y. Rocker, New York Press, Screw, and Bridal Guide. He has continued to contribute to comics anthologies such as Zero Zero.

Kaz has also worked on several animated television shows including SpongeBob SquarePants, Camp Lazlo, and Phineas and Ferb. He was co-executive producer of Get Blake!.

Kaz joined SpongeBob SquarePants as a storyboard director and writer in 2001 during the production of the series' third season and was paired with C. H. Greenblatt. The series went on hiatus after production began on The SpongeBob SquarePants Movie. Shortly before production on the fourth season began in 2004, Kaz was invited by his colleague and the series' newly appointed showrunner, Paul Tibbitt, to work on an episode for the fourth season but he was never contacted by Tibbitt again and joined Camp Lazlo after leaving SpongeBob. After Phineas and Ferb ended production, Kaz returned to SpongeBob in 2015 as a writer.

With Derek Drymon, Kaz co-wrote and storyboarded the pilot episode for Diggs Tailwagger, which was ultimately not picked up. In September 2006, Kaz left Camp Lazlo to work on another pilot for a Cartoon Network show, Zoot Rumpus, based on a character from Underworld. With Mr. Lawrence, he wrote the episode SpongeBob's Big Birthday Blowout and is currently working on the first SpongeBob spinoff, Kamp Koral. He also serves as a writer and outliner on the second spinoff, The Patrick Star Show.

Kaz will write the screenplay for the Sandy Cheeks spinoff film, Saving Bikini Bottom: The Sandy Cheeks Movie, which Tom Stern will also write the film with him.

Personal life
Kaz lives in Hollywood, California, with his wife Linda Marotta. Kaz is of Lithuanian descent.

title: Kaz (cartoonist)


text:
Talk:Perianth

Disambig
If you think this should be a disambiguation page, then do not change links to it. I will revert back to a redirect shortly, unless you can justify, but remember: Wikipedia is not a dictionary and a page with just definitions should be a redirect unless needed to sort out two or more common uses of the same term. I do not think that is the case here. - Marshman 01:53, 11 October 2005 (UTC)

 * I disagree. Not only does perianth have several separate possible meaning (flowering plants, liverworts), in flowering plants it is also a superterm. The previous redirect was like redirecting the term "automobile" to "pickup truck". G.Hagedorn (talk) 23:39, 12 August 2011 (UTC)

 * Can this be elaborated a bit more then? Aditya (talk • contribs) 12:34, 28 January 2012 (UTC)

title: Talk:Perianth


text:
New Forest and Christchurch (UK Parliament constituency)

New Forest and Christchurch was a county constituency in Hampshire which elected one Member of Parliament (MP) to the House of Commons of the Parliament of the United Kingdom. It was created for the 1918 general election, partially replacing the previous New Forest constituency, and was abolished for the 1950 general election, when it was partially replaced by a recreated New Forest constituency.

Boundaries
The Boroughs of Christchurch, Lymington, and Romsey, and the Rural Districts of Christchurch, Fordingbridge, Lymington, New Forest, Ringwood, and Romsey.

Elections in the 1930s
General Election 1939–40: Another General Election was required to take place before the end of 1940. The political parties had been making preparations for an election to take place and by the Autumn of 1939, the following candidates had been selected;
 * Conservative: John Mills
 * Liberal: H J Dey
 * Labour: RE Gray


text:
Talk:Richard Gordon

Untitled
Does this page need some disambiguification? Specifically, was the school Snoopy`s creater attended named after the astronaut later? Or is there another Richard Gordon worthy of note? Andycjp October 2005

title: Talk:Richard Gordon


text:
Wikipedia:Articles for deletion/Joey Uresti

 * The following discussion is an archived debate of the proposed deletion of the article below. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or on a Votes for Undeletion nomination).  No further edits should be made to this page.

The result of the debate was delete --Cel e stianpower hablamé 17:36, 17 October 2005 (UTC)

Joey Uresti
Y'know, after my first full day as an admin, it feels really weird to be nominating such a blatantly worthless article for deletion instead of just deleting it myself. But the article does claim noteworthiness (despite Google not knowing the name at all), so nn-bio doesn't apply. DS 01:54, 11 October 2005 (UTC)
 * Delete nonsense article, vanity page and or not notable, you pick it.--MONGO 02:13, 11 October 2005 (UTC)
 * Delete as hoax. Grammy Award winners and performers of #1 hits are notable per WP:MUSIC, but the person actually has to have accomplished those things, not just make up claims to having done so. --Metropolitan90 02:25, 11 October 2005 (UTC)
 * Delete if someone wants to source those claims I might reconsider, but until then, he seems thoroughly nn. -Greg Asche (talk) 02:29, 11 October 2005 (UTC)
 * Delete as hoax. People who achieve any position on the US charts let alone #1 or win Grammys tend to have comprehensive Allmusic.com articles. This fellow doesn't have an Allmusic.com article. They also tend to Google well. This fellow has two results relating to a Christina Aguilera guestbook. Unfortunately, that is as close as he gets to meeting WP:music. Capitalistroadster 03:21, 11 October 2005 (UTC)
 * Delete hoax. I guess this person read our WP:CSD and WP:MUSIC and learned to make a claim, knowing they'ld get a free web page for five days.  --rob 08:03, 11 October 2005 (UTC)
 * Delete as per above Qaz  ( talk ) 10:08, 11 October 2005 (UTC)
 * Delete hoax Jesse 14:14, 11 October 2005 (UTC)
 * Delete hoax CLW 15:19, 11 October 2005 (UTC)
 * Delete Hoax I googled PETA, Joe and Uresti and came up empty.Joaquin Murietta 22:54, 14 October 2005 (UTC)
 * The above discussion is preserved as an archive of the debate. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or in an undeletion request). No further edits should be made to this page.


text:
Jeremiah Weed

Jeremiah Weed is a brand of bourbon whiskey-based products. The Jeremiah Weed brand is owned and marketed by Diageo.

Range
Their offerings include a 90 proof blended whiskey distilled in Kentucky, and a bourbon-based 100-proof liqueur manufactured in Connecticut. In 2011, Jeremiah Weed entered the flavored malt beverages market with five blends, three marketed in the U.S. and two in the UK. The U.S.-market blends are 5.8% ABV, and the UK-market blends are 4.0% ABV.

In 2009, Jeremiah Weed introduced a blend of flavored vodka, Southern Style Sweet Tea, followed in 2010 by a lemonade blend called Half and Half. 2011 saw the introduction of three flavored malt beverages (a category sometimes referred to as alcopop) — Lightning Lemonade, Roadhouse Tea, and Spiked Cola.

Also in 2011, Jeremiah Weed launched two Brews into the UK: Jeremiah Weed Sour Mash Brew which has a bourbon taste and Jeremiah Weed Root Brew which has a ginger taste.

Promotion
Gary Jules produced a song titled "Jeremiah Weed" in 1998. The brand was also promoted by the folk rock band Dos Gringos in their 2003 song, "Jeremiah Weed" in which the product's stance as a favorite of United States Air Force fighter pilots is heavily referenced, as both of the singers are veteran F-16 Fighting Falcon pilots. Ohio folk singer Eric Nassau also performed a song with the same title in 2008.

Jeremiah Weed was promoted extensively by The Adam Carolla Podcast. American Southern rock band ZZ Top is also a current promoter of the brand, as shown in a video on Jeremiah Weed's YouTube page.

In 2012, Jeremiah Weed released its first TV commercial, "Alligator" exclusively in the United Kingdom. It was directed by The General Assembly (directors) in Los Angeles. The spot features a real 7-foot alligator.

In 2013, Diageo changed the advertising of Jeremiah Weed in the UK, including the Alligator advert to describe the product as a cider.

title: Jeremiah Weed


text:
Hať

Hať (formerly Haš; Haatsch) is a municipality and village in Opava District in the Moravian-Silesian Region of the Czech Republic. It has about 2,600 inhabitants. It is part of the historic Hlučín Region.

Geography
Hať is located about 23 km east of Opava and 12 km north of Ostrava, on the border with Poland. It lies mostly in the Opava Hilly Land, only the eastern part of the municipal territory extends into the Ostrava Basin. The highest point is at 279 m above sea level. The Bečva Stream flows through the municipality.

History
The first written mention of Hať is in a deed of Pope Innocent IV from 1250, when the village was owned by the monastery in Velehrad. From 1439, it was owned by various lower noblemen. In 1517–1567, Hať belonged to the Hlučín estate, then it was annexed to the Šilheřovice estate. In 1673, a large fire damaged the village. From 1742 to 1918, after Empress Maria Theresa had been defeated, the village belonged to Prussia. In 1920, it became part of the newly established Czechoslovakia.

In 1978–1990, Hať was an administrative part of Hlučín. Since 1990, it has been again an independent municipality.

Transport
There are no railways or major roads passing through the municipality.

Sights
The main landmark of Hať is the Church of Saint Matthew. It was built in the Baroque style in 1731 and rebuilt in 1894.

Notable people

 * Paul Billik (1891–1926), German fighter pilot

title: Hať


text: User talk:70.245.167.145

title: User talk:70.245.167.145


text: User talk:210.9.39.22

title: User talk:210.9.39.22


text:
Epicotyl

An epicotyl is important for the beginning stages of a plant's life. It is the region of a seedling stem above the stalks of the seed leaves of an embryo plant. It grows rapidly, showing hypogeal germination, and extends the stem above the soil surface. A common misconception is that the epicotyl, being closer to the apex of the plant, is the first part to emerge after germination - rather, the hypocotyl, the region of the stem between the point of attachment of the cotyledons and the root - forms a hook during hypogeal germination and pushes out of the soil, allowing the more delicate tissues of the plumules and apical meristem to avoid damage from pushing through the soil. The epicotyl will expand and form the point of attachment of the shoot apex and leaf primordia or "first true leaves". Cotyledons may remain belowground or be pushed up aboveground with the growing stem depending on the plant species in question.

In plant physiology, the epicotyl is the embryonic shoot above the cotyledons. In most plants the epicotyl will eventually develop into the leaves of the plant. In dicots, the hypocotyl is what appears to be the base stem under the spent withered cotyledons, and the shoot just above that is the epicotyl. In monocot plants, the first shoot that emerges from the ground or from the seed is the epicotyl, from which the first shoots and leaves emerge.

Lengthening of the epicotyl is thought to be controlled by the phytochrome photoreceptors.

title: Epicotyl


text:
File:Sinatraseptember.jpg

Summary
Cover of the 1965 Frank Sinatra album September of My Years.

title: File:Sinatraseptember.jpg


text:
Scientific Working Group – Bloodstain Pattern Analysis

The Scientific Working Group on Bloodstain Pattern Analysis (SWGSTAIN) was created in March 2002 at a meeting held by the FBI Laboratory at the FBI Academy in Quantico, Virginia. It was decided that there was enough interest in bloodstain pattern analysis (BPA) to warrant the creation of the Scientific Working Group (SWG). According to the guidelines for organizing a SWG, the Scientific Working Group on Bloodstain Pattern Analysis (SWGSTAIN) generated and ratified a set of bylaws in accordance to the Scientific Working Groups published in Forensic Science Communications (July 2002).

SWGSTAIN has nationally and internationally recognized bloodstain pattern analysts, several of whom are members of the International Association of Bloodstain Pattern Analysts (IABPA). The experts come from various areas including law enforcement, federal, state and local laboratories, the private sector, and academia. They also come from various countries including United States, Canada, England, and the Netherlands.

In 2004, the various sub-committees were discussing and drafting proposals in the following areas:

 * Terminology
 * Quality Assurance
 * Legal
 * Ethics
 * Education and Training

SWGSTAIN meets twice a year at the FBI Academy in Quantico. They have an American Society of Crime Laboratory Directors (ASCLD) representative.

Mission statement

 * To Promote and enhance the development of quality forensic bloodstain pattern (BSP) practices through the collaborative efforts of government forensic laboratories, law enforcement, private industry, and academia.

Objectives

 * 1) To discuss, share and compare stain pattern analysis methods, protocols, and research for the enhancement of forensic bloodstain pattern analysis (BPA) techniques, and
 * 2) To design and encourage the implementation by practitioners of a quality assurance program in bloodstain pattern analysis and to advise the forensic bloodstain pattern analysis community of emerging quality assurance issues, and
 * 3) To discuss and share strategies for presenting bloodstain pattern information to meet Frye, Daubert, or other jurisdictional admissibility challenges, and
 * 4) To address the development and/or validation of forensic bloodstain pattern analysis methods, and
 * 5) To design and encourage the adoption of guidelines to ensure the quality of specialized training in the field of bloodstain pattern analysis.

Executive board
The SWGSTAIN Executive Board consists of eight members:

 * Chair
 * Vice-Chair (must be a non-FBI SWGSTAIN member, appointed by the Chair)
 * Executive Secretary (appointed by the Chair, no voting privileges)
 * Five Regular Members


text: User talk:68.5.216.45

title: User talk:68.5.216.45


text:
Adolf Beck case

The Adolf Beck case was a notorious incident of wrongful conviction by mistaken identity, brought about by unreliable methods of identification, erroneous eyewitness testimony, and a rush to convict the accused. As one of the best known causes célèbres of its time, the case led to the creation of the English Court of Criminal Appeal in 1907.

Biographical background
Adolf (or Adolph) Beck was born in Norway in 1841, and educated as a chemist. However, he went to sea soon afterwards and moved to England in 1865, working as a clerk to a shipping broker. In 1868 he moved to South America, where he made a living for a while as a singer, then became a shipbroker, and also engaged in buying and selling houses. He soon amassed a considerable amount of savings, at one time earning £8,000 as commission for a sale of a Spanish concession in the Galapagos Islands. He returned to England in 1885 and engaged in various financial schemes, including an investment in a copper mine in Norway. Unfortunately the mine did not turn a profit, and he poured in more and more money until he had to put the mine up for sale. There were no takers and he was reduced to near-poverty. He was chronically short of money, in debt to the hotel in Covent Garden where he lived and had borrowed money from his secretary. Nevertheless, he tried to keep up appearances by dressing in a frock coat and top hat whenever he went out, even though they had become threadbare.

Arrest
On 16 December 1895 Beck was stepping out of the front door of 135 Victoria Street (or 139, according to at least one account) when a woman blocked his way. She accused him of having tricked her out of two watches and several rings. Beck brushed her aside and crossed the road. When the woman followed him, he complained to a policeman that he was being followed by a prostitute who had accosted him. The woman in turn demanded his arrest, accusing him of having swindled her three weeks earlier. The policeman took them both to the nearest police station, where the woman identified herself as Ottilie Meissonier, unmarried, and a language teacher. She alleged that she had been walking down Victoria Street when Beck approached her, tipping his hat and asking if she was Lady Everton. She said that she was not, but she was impressed by his gentlemanly manner and they struck up a conversation. According to her account, he introduced himself as "Lord Willoughby" and advised her that the flower show she was heading for was not worth visiting. He said that he knew horticulture because he had gardens on his Lincolnshire estate which were extensive enough to require six gardeners. Meissonier mentioned that she grew chrysanthemums; he asked her whether he might see them and she invited him to tea the following day.

At her home the next day, he invited her to go to the French Riviera on his yacht. He insisted upon providing her with an elegant wardrobe for the voyage, wrote out a list of items for her and made out a cheque for £40 to cover her purchases. Then he examined her wristwatch and rings, and asked her to let him have them so that he could match their sizes and replace them with more valuable pieces. After he left, she discovered that a second watch was missing. Suspicious, she hurried to the bank to cash the cheque, only to find that it was worthless. She had been swindled and she swore that it was Adolf Beck who had done it. He was promptly arrested.

The inspector who was assigned to the case learned that in the previous two years twenty-two women had been defrauded by a grey-haired man who called himself "Lord Wilton de Willoughby" and used the same modus operandi as Beck's accuser had described. These women were asked to view a line-up that included Beck along with ten or fifteen men who had been selected randomly from the street. Because he was the only one with grey hair and a moustache he was quickly identified by the women as the man who had defrauded them.

Beck was charged with ten misdemeanours and four felonies. The felony charges were based on presumed prior convictions in 1877, when a man named John Smith had been sentenced to five years for swindling unattached women by using the name Lord Willoughby, writing worthless cheques and taking their jewellery. He had disappeared after his release, and it was assumed that Beck and Smith were one and the same. Descriptions of John Smith from prison files were never compared with the current appearance of Adolph Beck.

At Beck's committal hearing, in late 1895, one of the policemen who had arrested Smith eighteen years before was called to testify. Eless Henry Spurrell (1847-1906), who had retired in 1892, gave his account as follows:

"In 1877 I was [a PC] in the Metropolitan Police Reserve [of E Division]. On 7 May 1877 I was present at the Central Criminal Court where the prisoner in the name of John Smith was convicted of feloniously stealing ear-rings and a ring and eleven shillings of Louisa Leonard and was sentenced to five years' penal servitude. I produce the certificate of that conviction. The prisoner is the man. ... There is no doubt whatever – I know quite well what is at stake on my answer and I say without doubt he is the man."

Beck protested and insisted that he could bring witnesses from South America to prove that he was there in 1877.

Trial
On 3 March 1896 Beck was brought to trial at the Old Bailey. The Crown was represented by Horace Edmund Avory, assisted by Guy Stephenson, while the defence was headed by an experienced barrister, Charles Gill, who was assisted by Percival Clarke. The judge was Sir Forrest Fulton, who, as a prosecutor, had been responsible for sending John Smith to prison in 1877.

The defence's strategy was to argue that this was a case of mistaken identity. If they could prove that Beck was in South America at the time when John Smith was committing his crimes and went to prison for them, they could undermine the allegation that Adolph Beck was John Smith.

A handwriting expert named Thomas Gurrin compared the lists of clothing Smith had given his victims in 1877 to those written in 1894 and 1895, as well as to samples of Beck's handwriting. Gill thought that he would have his chance to prove mistaken identity when he cross-examined Gurrin. If Gurrin testified in court, as he had said previously, that the writing from 1877 was identical to that from 1894 and 1895, Gill could bring witnesses to show that Beck had been in Buenos Aires in 1877. Avory, foreseeing this tactic, asked the witness only about the later lists. Gurrin said that these had been written by Beck with a "disguised hand". Gill then asked Justice Fulton's permission to question Gurrin about the lists from 1877, but he ruled, in line with procedure in the English courts, that any earlier convictions of the defendant could not be mentioned in court until after the jury had given its verdict.

Avory did not want to call Elless Spurrell to give evidence because his testimony would have opened discussion of the past conviction, thereby allowing Gill the opportunity to cast doubt on Beck's guilt. Without Spurrell's testimony, Avory could still prosecute Beck for the misdemeanours, which did not require proof of prior conviction. He chose not to proceed with the felony charges, despite the fact that the prosecution case was based wholly on the unstated premise that Adolph Beck and John Smith were the same person.

Avory brought Beck's alleged victims into court and one after another they pointed to Beck as the swindler. There were, however, occasional moments of doubt. One mentioned that the swindler talked differently from Beck, peppering his speech with "Yankee" slang. Ottilie Meissonier remembered that the swindler had a scar on the right side of his neck, but was otherwise convinced that Beck was the man. Another testified that his mustache was longer and was waxed.

Conviction and doubts
On 5 March 1896 Adolf Beck was found guilty of fraud and was sentenced to seven years of penal servitude at Portland Convict Prison on the Isle of Portland. In prison he was given John Smith's old prison number, D 523, with the letter W added, indicating a repeat convict.

England did not yet have a court of criminal appeal, but between 1896 and 1901 Beck's solicitor presented ten petitions for re-examination of his case. His requests to see the prison's description of John Smith were repeatedly denied. However, in May 1898 an official at the Home Office looked at the Smith file and saw that Smith was Jewish and thus had been circumcised, while Beck was not. The Home Office asked Sir Forrest Fulton for his opinion of this new evidence. Fulton wrote a minute dated 13 May in which he acknowledged that Smith and Beck could not be the same person but he added that, even if Beck was not Smith, he was still the impostor of 1895, and that he viewed the South American alibi "with great suspicion." As a result, the letter W was removed from Beck's prison number, but nothing else was done regarding the case.

While Beck remained in prison, George Robert Sims, a journalist who worked for the Daily Mail and had known Beck since his return to England in 1885, wrote an article in the paper emphasising that Beck had been tried on the assumption that he and Smith were the same person, yet no evidence to support that assumption had been allowed by Judge Fulton. Public opinion was slowly swayed by Sims and others, including Arthur Conan Doyle, to the view that Beck's conviction was unjust.

Beck was paroled in July 1901 for good behaviour.

Second arrest and conviction
On 22 March 1904, a servant by the name of Paulina Scott filed a complaint that a grey-haired, distinguished looking man had accosted her on the street, paid compliments to her and then stolen her jewellery. The inspector who took the complaint was familiar with Beck's case and assumed he must be the culprit, so he sent Scott to the restaurant where Beck took his lunch. She did not recognise him but the inspector was undeterred by the woman's uncertainty and set a trap for him.

On 15 April 1904, as Beck left his flat, Scott ran up to him and accused him of defrauding her of her jewellery. Beck was horrified and denied the charge. Scott repeated her accusations and told him that someone was waiting to arrest him. He ran away in panic, but was caught immediately by the waiting police inspector, who arrested him at once. Beck's panicked flight reinforced the inspector's assumption regarding his guilt.

He was again put on trial on 27 June at the Old Bailey before Sir William Grantham. Five women identified him and, based on this positive identification, he was found guilty by the jury. The judge, however, was dissatisfied about the case and expressed some doubts regarding it. Despite assurances from the Home Office and the police of Beck's guilt, he decided to postpone sentencing. Ten days later the case was solved once and for all.

Truth about John Smith
On a routine visit to the Tottenham Court Road police station on 7 July, Inspector John Kane of the Criminal Investigation Department was told of the arrest of a man who had tried to swindle some rings from a pair of unemployed actresses that afternoon and had been apprehended at a pawnshop. The detective was familiar with the Beck case, having been present at Beck's two trials and asked for details. The details fitted the usual pattern but the alleged culprit, Adolph Beck, was already in jail, awaiting sentencing.

The inspector went to the new prisoner's cell. It held a grey-haired man, approximately of Beck's height, with certain features which made him resemble Beck. However, Beck was younger and frailer in build, and this man had a scar on the right side of his neck, as Ottilie Meissoner remembered. The prisoner had given his name as William Thomas but the inspector, convinced that he was John Smith, informed Scotland Yard. Three of the five women who identified Beck in his second trial were brought in to confront Thomas and they quickly identified him as the swindler (the other two had gone abroad and thus were not present). Other swindled women were brought in who also admitted their error in identifying Beck. When the man who had been John Smith's landlord in 1877 identified Thomas as his former tenant, the prisoner confessed his crimes.

"William Thomas" turned out to be as much an alias as "John Smith" had been, and he had two other aliases as well, "William Wyatt" and "William Weiss". His true identity was Wilhelm Meyer, born in Vienna and graduated from the University of Vienna. He studied leprosy in the Hawaiian Islands under Father Joseph Damien. He later became surgeon to the King of Hawaii and was engaged in growing coffee, and in various other businesses in the United States, then setting up practice as a physician in Adelaide before moving to London. Apparently he fell upon hard times there, and turned to preying on women through fraud. When Beck was sent to prison in his place, Meyer had returned to the United States and did not come back until 1903, apparently when he thought Beck had served out his sentence. Thomas then resumed his swindling until he was finally arrested. When brought to trial on 15 September, Wilhelm Meyer pleaded guilty to those offences and was jailed for 5 years.

Aftermath
Adolf Beck was given a free pardon by the King on 29 July 1904 and in compensation for his false imprisonment was awarded £2,000, later raised to £5,000 due to public clamour (about £600,000 as of May 2023), again due to George Robert Sims, but those who were responsible were the subject of public indignation.

Eventually, a Committee of Inquiry was established, headed by the noted jurist and Master of the Rolls, Sir Richard Henn Collins. It heard evidence from all those involved in the case, including Horace Avory and Sir Forrest Fulton. In its report, it concluded that Adolph Beck should not have been convicted due to the errors made by the prosecution. The committee also chastised Judge Fulton in his conduct of the case, as he should have given consideration to the 1877 case, more so because of his involvement with it, which served to prejudice the proceedings against Beck. Furthermore, it criticised the Home Office for its indifference in acting on the case despite knowing since 1898 that Beck and Smith were not the same man. Instead, it sought to preserve the credibility of the judiciary rather than admit or correct its mistakes. It also stated that the omission of the prison authorities to state the fact of Smith's circumcision in the records of 1877 and 1881 was the primary cause of the miscarriage of justice.

As a direct result of the case, important reforms resulted, including the creation of the Court of Criminal Appeal. The case is still cited by judges in Commonwealth countries as a glaring example of how inaccurate eyewitness identification can be, and the extreme care with which juries must regard evidence of this kind. As for Adolf Beck, his exoneration brought him little consolation. He died a broken man of pleurisy and bronchitis in Middlesex Hospital on 7 December 1909.

title: Adolf Beck case


text: User talk:69.129.17.185

title: User talk:69.129.17.185


text: User talk:68.81.86.254

title: User talk:68.81.86.254


text: User talk:71.34.215.128

title: User talk:71.34.215.128


text:
Healtheon

Healtheon was a dot-com company founded by James H. Clark and Pavan Nigam. The company's mission was to "use the power of computing and the Internet to revolutionize the healthcare industry, stripping away its inefficiencies and inequities and streamlining it for the new millennium".

In 1999, the company was acquired by WebMD.

History
In mid-1995, James H. Clark, the founder of Netscape, came up with the idea to modernize technology in the health care industry. He founded Healthscape in early 1996 with funding from Kleiner Perkins Caufield & Byers. To avoid confusion with Netscape, the company changed its name to Healtheon.

The company's first big idea was to develop a system for linking insurers and human resources departments. However, the idea failed since insurers dismissed it as too expensive and human resource departments were not interested.

In 1997, Mike Long became chief executive officer of the company. Five months later, the company formed a research and development partnership with Brown & Toland, a network of 1,600 physicians in San Francisco.

in February 1998, the company announced the acquisition of ActaMed, a medical-records clearinghouse for doctors and insurers, for $150 million, which gave the company a source of revenue.

In August 1998, the company filed for an initial public offering, but the offering was cancelled in October 1998, after stock prices dropped due to the 1998 Russian financial crisis.

In February 1999, the company completed its IPO and became a public company and the stock price rose 400% on its first day of trading.

On April 21, 1999, the company announced the acquisition of MedE America for $478 million in stock.

On May 20, 1999, the company announced a merger with WebMD.

title: Healtheon