Patterson syndrome is characterized by the patient’s having an unusual facial look, similar to that caused by Leprechaunism. It primarily affects the connective tissue and the neuroendocrine system, giving rise to bronzed hyperpigmentation, cutis laxa of the hands and feet, bodily disproportion, severe mental retardation, and major bony deformities. Radiographs reveal a characteristic generalised skeletal dysplasia.

It comprises endocrine abnormality, hyperadrenocorticism, cushingoid features, and diabetes mellitus. One other case has shown premature adrenarche.

The pathogenesis and etiology of the Patterson syndrome was unknown as of 1981.

References

• Journal of Medical Genetics, 1981, Vol 18, 294-298 PMID 7277424
• Patterson, J. H.; Watkins, W. L., “Leprechaunism in a male infant.” J. Pediat. 60: 730-739, 1962. PMID 14484402
• Patterson Pseudoleprechaunism Syndrome,

A specificity of the TDT is that it will detect genetic linkage only in the presence of genetic association.
While genetic association can be caused by population structure, genetic linkage will not be affected which makes the TDT robust to the presence of population structure.

The case of trios: one affected child per family

Description of the test

We first describe the TDT in the case where families consist of trios (two parents and one affected child). Our description follows the notations used in Spielman, McGinnis & Ewens (1993).

The TDT measures the over-transmission of an allele from heterozygous parents to affected offsprings.
For a set of <math> n </math> heterozygous parents with alleles <math> M_1 </math> and <math> M_2 </math> at a genetic locus, each parent can be summarized by the transmitted and the non-transmitted allele. Summarizing the data in a 2 by 2 table gives:

</tr>

</table>
</center>

The derivation of the TDT shows that one should only use the heterozygous parents (total number b+c).
The TDT tests whether the proportions <math> b/(b+c) </math> and <math> c/(b+c) </math> are compatible with probabilities <math> (0.5, 0.5) </math>.
This hypothesis can be tested using a binomial (asymptotically chisquare) test with one degree of freedom:

<math> \chi^2 = \frac{ [b - (b+c)/2]^2}{(b+c)/2} + \frac{ [c - (b+c)/2]^2}{(b+c)/2} = \frac{(b-c)^2}{b+c} </math>

Outline of the test derivation

A derivation of the test consists of using a population genetics model to obtain the expected proportions for the quantities <math> a,b,c </math> and <math> d </math> in the table above. In particular, one can show that under nearly all disease models the expected proportion of <math> b </math> and <math> c </math> are identical. This result motivates the use of a binomial (asymptotically <math> \chi^2 </math>) test to test whether these proportions are equal.

On the other hand, one can also show that under such models the proportions <math> a,b,c </math> and <math> d </math> are not equal to the product of the marginals probabilities <math> a+b/2n</math>, <math> c+d/2n </math> and <math> a+c/2n </math>, <math> b+d/2n </math>. A rewording of this statement would be that the type of the transmitted allele is not, in general, independent of the type of the non-transmitted allele. A consequence is that a <math> \chi^2 </math> test for homogeneity/independence does not test the appropriate hypothesis, and thus, only heterozygous parents are included.

Extension to two affected child per family

Extension of the test

The TDT can be readily extended beyond the case of trios. We keep following the notations of Spielman, McGinnis & Ewens (1993). Let us consider a total of <math> h </math> heterozygous parents. We use the fact that the transmissions to different children are independent. The information can be then summarized in three categories:

<math> i </math> = number of parents who transmit <math> M_1 </math> to both children.
<math> h-i-j </math> = number of parents who transmit <math> M_1 </math> to one child and <math> M_2 </math> to another.
<math> j </math> = number of parents who transmit <math> M_2 </math> to both children.

Using the notations of the previous paragraph we have:
<math> b = 2i + (h-i-j) = h + i - j </math>
<math> c = 2j + (h-i-j) = h - i + j </math>
leading to the <math> \chi^2 </math> test statistic:
<math> \chi_{tdt}^2 = \frac{2(i-j)^2}{h} </math>

Relation with another linkage statistic

The comparison with the more traditional (at least at the time when the TDT was proposed) linkage test proposed by Blackwelder and Elston 1985 is informative.
The Blackwelder and Elston approach uses the total number of haplotypes identical by descent (mean haplotype sharing). This measure ignores the allelic state of a marker and simply compares the number of time a parent transmits the same allele to both affected children with the number of times a different allele is transmitted.
The test statistic is:
<math> \chi^2_{hs} = \frac{(2i+2j-j)^2}{h} </math>

Under the null hypothesis of no linkage the expected proportions of <math> (i, h-i-j, j) </math> are <math> (0.25, 0.5, 0.25) </math>.
One can derive a simple <math> \chi^2 </math> statistic with 2 degrees of freedom:

<math> \chi^2_{total} = \frac{(i - h/4)^2}{h/4} + \frac{(h-i-j-h/2)^2}{h/2} + \frac{(j-h/4)^2}{h/4} = \chi^2_{tdt} + \chi^2_{hs}</math>

It clearly appears that the total statistic (with two degree of freedom) is the sum of two independent components: one is the traditional linkage measure and the other is the TDT statistic.

A modified version of the TDT

More recently, Wittkowski KM, Liu X. (2002/2004) proposed a modification to the TDT that can be more powerful under some alternatives, although the asymptotic properties under the null hypothesis are equivalent.

The motivating idea for this modification is the fact that, while the transmissions of both allele from parents to a child are independent, the effects of other filial genetic or environmental covariates on penetrance are the same for both alleles transmitted to the same child. This situation can be important if, for example, the genetic marker is linked to a disease locus with a strong selection against heterozygous individuals. This observation suggests to shift the statistical model from a set of independent transmissions to a set of independent children (see Sasieni (1997) for the corresponding problem in case-control association tests). While this observation does not affect the distribution under the null hypothesis of no linkage, it allows, for some disease models, to design a more powerful test.

In this modified TDT test the children are stratified by parental type and the modified test statistic becomes:

<math> \chi^2 = \frac{ \left[ [n_{PQ} - n_{QQ}]_{PQ \sim QQ} + 2\times[n_{PP} - n_{QQ}]_{PQ \sim PQ} + [n_{PQ} - n_{QQ}]_{PP \sim PQ} \right]^2}{[n_{PQ} + n_{QQ}]_{PQ \sim QQ} + 4\times[n_{PP} + n_{QQ}]_{PQ \sim PQ} + [n_{PQ} + n_{QQ}]_{PP \sim PQ}}
</math>

where <math> [n_{PQ}]_{PQ \sim QQ} </math> is the number of PQ children from parents with the PQ and QQ types.

References

• Ewens WJ, Spielman RS. (2005) What Is the Significance of a Significant TDT? Hum Hered. 60(4):206-10.
• Wittkowski KM, Liu X. (2002/2004) A statistically valid alternative to the TDT Hum Hered. 54(3):157-64. Comment, author reply, discussion Hum Hered. 58(1):59-62.
• Spielman RS, Ewens WJ. (1998) A sibship test for linkage in the presence of association: the sib transmission/disequilibrium test. Am J Hum Genet. 62(2):450-8.
• Sasieni PD. (1997) From genotypes to genes: doubling the sample size. Biometrics. 53 (4):1253-61.
• Spielman RS, Ewens WJ. (1996) The TDT and other family-based tests for linkage disequilibrium and association. Am J Hum Genet 59:983-9
• Ewens WJ, Spielman RS. (1995) The transmission/disequilibrium test: history, subdivision, and admixture. Am J Hum Genet. 57(2):455-64.
• McGinnis RE, Ewens WJ, Spielman RS. (1995) The TDT reveals linkage and linkage disequilibrium in a rare disease. Genet Epidemiol. 12(6):637-40.
• Spielman RS, McGinnis RE, Ewens WJ. (1993) Transmission test for linkage disequilibrium: the insulin gene region and insulin-dependent diabetes mellitus (IDDM). Am J Hum Genet. 52(3):506-16.

A Conquistador (Spanish: []) (English: Conqueror) was a Spanish soldier, explorer and adventurer who took part in the gradual invasion and conquering of much of the Americas and Asia Pacific, bringing them under Spanish colonial rule between the 15th and 19th centuries.

• Spanish colonization of the Americas
• Encomienda
• Repartimiento
• List of conquistadors
• New Laws
• Valladolid debate
• Bandeirantes

References

• John Charles Chasteen, Born In Blood And Fire: Concise History of Latin America Summary of the history of Latin America.
• The Conquistadors - Start the Adventure (PBS): http://www.pbs.org/opb/conquistadors/home.htm

Etiology

17-beta-hydroxysteroid dehydrogenase deficiency type 3 (17βHSD3) is a disorder in testosterone biosynthesis. As a consequence of this disorder, normal male sexual differentiation in impaired and hypovirilization occurs (less male sexual characteristics).

Clinical characteristics

17-beta-hydroxysteroid dehydrogenase deficiency-3 is clinically characterized by either ambiguous external genitalia or complete female external genitalia at birth as a consequence of impaired male sexual differentiation in 46,XY individuals. Further investigations on ambiguous genitalia will eventually lead to findings of intersexuality. Severe hypovirilization (absence of male differentiation) can lead to development of female external genitalia. These females (!) are often discovered when there is absence of menarche (first menstruation) and when they begin to virilize during puberty (slowly become more like a man; deepening of the voice, acne, male musculature etc). At careful examination, testis can often be found in the inguinal channel.

Biochemically

17-beta-hydroxysteroid dehydrogenase deficiency-3 is biochemically characterized by decreased levels of testosterone and increased levels of androstenedione as a result of the defect in conversion of androstenedione into testosterone. This leads to clinically important higher ratio of androstenedione to testosterone (A’dion/T).-

Genetics

17-beta-hydroxysteroid dehydrogenase deficiency-3 is caused by gene mutations found in the 17BHSD3 gene. 17-beta-hydroxysteroid dehydrogenase deficiency-3 is an autosomal recessive disorder.

External links

References

Reaction to insulin

In the absence of insulin, GLUT4 is sequestered in the interior of muscle and fat cells.

Insulin induces the redistribution of GLUT4 from intracellular storage sites to the plasma membrane.

Once at the cell surface, GLUT4 facilitates the passive diffusion of circulating glucose down its concentration gradient into muscle and fat cells.

Once inside cells, glucose is rapidly phosphorylated by hexokinase to form glucose-6-phosphate, which then enters glycolysis.

Glucose-6-phosphate cannot diffuse back out of cells, which also serves to maintain the concentration gradient for glucose to passively enter cells.

Pathway

The pathway in which GLUT4 is expressed on the plasma membrane begins with insulin binding to the receptor in its dimer form. The receptor phosphorylates and subsequently activates IRS-1, which converts PIP2 to PIP3. PIP3 is bound to PKB (protein kinase B), signaling for PDK1 to phosphorylate PKB. Once phosphorylated, PKB is in its active form and phosphorylates other targets that stimulate GLUT4 to be expressed on the plasma membrane.

Contraction

Contraction also stimulates the cell to translocate GLUT4 receptors to the surface. This is especially true in cardiac muscle, where continuous contraction can be relied upon; but is observed to a lesser extent in skeletal muscle.

References

External links

See also

• Affectional action
• Forms of activity and interpersonal relations
• Instrumental action
• Tradition
• Traditional authority
• Value-rational action

External links

• “The Catenet Model for internetworking” (Cerf, V., DARPA Information Processing Techniques Office, IEN 48, July 1978.)

The term diabetologist is used in several ways. In North America over the last 40 years it is most often used for an internist who through practice and interest develops expertise in diabetes care without having formal training or board certification in endocrinology. Diabetology is not a recognized medical specialty and has no formal training programs leading to board certification. In other contexts the term diabetologist refers to any physician, including endocrinologists, whose practice and/or research efforts are concentrated mainly in diabetes care.

Apart from regulating medication (e.g. insulin) dosage and timing, a diabetologist will also concern himself with the potential consequences of diabetes, e.g. retinopathy, nephropathy and peripheral neuropathy.

See also

• Diabetologists

External links

• American Diabetes Association

In alchemy, congelation is one of the 12 vital processes for transformation to occur.

Clinical presentation

• proximal muscle wasting and tenderness of thigh muscles
• loss of knee reflexes
• seen in older men with diabetes
• frequently CSF(cerebrospinal fluid)protein is elevated
• usually occurs when diabetes is poorly controlled and resolves with good control ie the condition is reversible.

References

• Kumar & Clark. Clinical Medicine. 5th edition, pg. 1098.

Biography

Johnson was born in Beverly Hills, California. Her grandfather Robert Wood Johnson founded Johnson & Johnson care. She is first cousin of Jamie Johnson who directed the documentary “Born Rich”.

Personal Life

Dubbed ‘the Band-Aid Princess’, she was often seen partying with pals Paris Hilton, Nicky Hilton, and formerly Bijou Phillips. Johnson made headlines in June 2004 for being apart of an assault towards Nicole Marie Lenz along with Phillips. Then sueing Phillips herself for $500,000 later to be dropped. As of 2007 Johnson has plans on adopting a baby from Kazakhstan saying, “I’m going to dress her in the cutest leoapord bikini”.

Health

Was diagnosed with juvenile diabetes when she was eight, and has long been involved with the Juvenile Diabetes Foundation, working to promote awareness of the disease. She co-wrote a book when she was 14 about diabetes management.

C-peptide is the abbreviation for “connecting peptide”, although its name was probably also inspired by the fact that insulin is also composed of an “A” chain and a “B” chain. C-peptide was discovered in 1967. The first documented use of the C-peptide test was in 1972. It should not to be confused with c-reactive protein or Protein C.

Function

C-peptide functions in repair of the muscular layer of the arteries.

C-peptide also exerts beneficial therapeutic effects on many complications associated with diabetes mellitus http://www.pancreasjournal.com/pt/re/pancreas/abstract.00006676-200410000-00009.htm;jsessionid=GFMCZSW85zYmQt5bZ2BBkz2mF2KWKfm1FJ3XGx93KFYwQfSFtKL4!1152499061!181195629!8091!-1 , http://www.sciencemag.org/cgi/content/full/277/5325/531, such as for instance diabetic neuropathyhttp://diabetes.diabetesjournals.org/cgi/content/abstract/55/12/3581 and other diabetes-induced ailments. In the kidneys, C-peptide prevents diabetic nephropathy http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10784221&dopt=AbstractPlus, http://ndt.oxfordjournals.org/cgi/content/abstract/20/3/532, and in the heart http://diabetes.diabetesjournals.org/cgi/content/abstract/51/10/3077 blood flow is improved in diabetic patients.

In spite of these physiological functions, C-peptide is actually removed from pharmaceutical preparations of insulin sold by drug companies when they manufacture the synthetic human insulin that is in widescale clinical usage today.

Uses

• Newly diagnosed diabetes patients often get their C-peptide levels measured, to find if they are type 1 diabetes or type 2 diabetes. The reason that the C-peptide levels are measured instead of the insulin levels themselves is because insulin concentration in the portal vein ranges from two to ten times higher than in the peripheral circulation. The liver extracts about half the insulin reaching it (the plasma), but this varies with the nutritional state. The pancreas of patients with type 1 diabetes is unable to produce insulin and they will therefore usually have a decreased level of C-peptide, while C-peptide levels in type 2 patients is normal or higher than normal. Measuring C-peptide in patients injecting insulin can help to determine how much of their own natural insulin these patients are still producing.
• C peptide is also used for determining the possibility of gastrinomas associated with Multiple Endocrine Neoplasm syndromes (MEN 1). Since a significant amount of gastrinomas also include MEN which include pancreatic, parathyroid, and pituitary adenomas, higher levels of c-protein in addition to a gastrinoma may suggest other organs than just the stomach may include neoplasms.
• Can be used for identifying malingering: hypoglycemia with low C-peptide level may indicate abuse of insulin.

C-peptide levels are also checked to determine how insulin resistant women with Polycystic Ovarian Syndrome may be.

References

In mammals, transketolase connects the pentose phosphate pathway to glycolysis, feeding excess sugar phosphates into the main carbohydrate metabolic pathways. Its presence is necessary for the production of NADPH, especially by the brain. Thiamine diphosphate is an essential cofactor, along with calcium.

Diagnostic use

Red cell transketolase activity is reduced in deficiency of thiamine (vitamin B1), and may be used in the diagnosis of Wernicke’s encephalopathy and other B1-deficiency syndromes if the diagnosis is in doubt.Smeets EHJ, Muller A, de Wael J. A NADH-dependent transketolase assay in erythrocyte hemolysates. Clin Chim Acta 1971;33:379–386. PMID 4330339. Apart from the baseline enzyme activity (which may be normal even in deficiency states), acceleration of enzyme activity after the addition of thiamine pyrophosphate may be diagnostic of thiamine deficiency (0-15% normal, 15-25% deficiency, >25% severe deficiency).Doolman R, Dinbar A, Sela B. Improved measurement of transketolase activity in the assessment of TPP effect. Eur J Clin Chem Clin Biochem 1995;33:445–446. PMID 7548453.

References

This older method (prior to the development of long-acting insulin analogs and blood glucose monitoring) is still in use in a proportion of cases.

Conventional insulin therapy has these characteristics:

• Insulin injections of a mixture of rapid and intermediate acting insulin are performed two or three times daily.
• Meal are scheduled to match the anticipated peaks in the insulin profiles.
• The target range for blood glucose levels is higher than is desired in the intensive regimen. *Frequent measurements of blood glucose levels were not used.

The down side of this method is the fact that it is difficult to achieve as good results of glycemic control as with intensive insulinotherapy.

External links

• Gandalf home page

Ketoacidosis should not be confused with ketosis, which is one of the body’s normal processes for the metabolism of body fat. In ketoacidosis, the accumulation of keto acids is so severe that the pH of the blood is substantially decreased.

Pathophysiology

Ketoacidosis occurs when cells do not have sufficient glucose to meet their metabolic demands. Instead, ketone bodies are produced for energy via the metabolism of fatty acids.

Acidity results from the dissociation of the H⁺ ion at physiological pH of metabolic ketone bodies such as acetoacetate, and β-hydroxybutyrate.

Etiology

Two common causes include diabetic and alcoholic ketoacidosis.

In diabetic patients, ketoacidosis is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Since insulin is required to absorb glucose from the blood, its deficiency results in an energy crisis, fatty acid metabolism, and production of ketone bodies. Hyperglycemia results in glucose overloading the nephron and spilling into the urine. Dehydration results following the osmotic movement of water into urine, exacerbating the acidosis.

In alcoholic ketoacidosis, alcohol causes dehydration and blocks the first step of gluconeogenesis. The body is unable to synthesize enough glucose to meet its needs, thus creating an energy crisis resulting in fatty acid metabolism, and ketone body formation.

See also

• Diabetic ketoacidosis
• Keto acids
• Low-carbohydrate diet

External links

• The Merck Manual - Diabetic Ketoacidosis
• Alcoholic Ketoacidosis
• Lancet case study Atkins diet-induced Ketoacidosis

When such a possession occurs, the shaman is called. A hut is built in which the afflicted resides along with the shaman and his assistants until he is cured. For ten days or a fortnight these people eat and drink at the expense of the patient’s relatives, and dance to the music of flute and drum. Mbwiri is said to abhor good living, and this is the best way to drive him out. The patient will be the only one who knows that he is possessed. The patient also dances until the epileptic fits come on. When he is pronounced cured, he builds a little fetish house, and thenceforth avoids certain kinds of food and performs certain duties. Sometimes, however, the process appears to result in madness, and some patients run away into the bush.

• 1 Language
• 2 Logic
• 3 Cartography
• 4 External links
• 5 See also

Language

In language, idiom conflation is the amalgamation of two different expressions. In most cases, the combination results in a new expression that makes little sense literally, but clearly expresses an idea because it references well-known idioms. All conflations fit into one of two major categories: congruent conflations and incongruent conflations.

Congruent conflations are the more ideal (and more sought-after) examples of the concept. These occur when the two root expressions basically reflect the same thought. For example, “Look who’s calling the kettle black” can be formed using the root expressions “Look who’s talking” and “The pot is calling the kettle black.” These root expressions really mean the same thing—they are both a friendly way to point out hypocritical behaviour. Of course, without reference to a pot (which is just as black as a kettle), “Look who’s calling the kettle black” does not directly imply anything. Yet the implication is almost automatically understood because the conflation clearly refers to two known idioms.

Incongruent conflation occurs when the root expressions do not mean the same thing, but share a common word or theme. For example, “a bull in a candy shop” can be formed from the root expressions “a kid in a candy shop” and “a bull in a china shop.” The former root expression paints a picture of someone who is extraordinarily happy and excited, whereas the latter root brings to mind the image of a person who is extremely clumsy. The conflation potentially expresses both of these ideas at the same time without making the speaker’s intention entirely clear.

Logic

In logic, conflation is the error of treating two distinct concepts as if they were one. The result of conflating concepts may give rise to fallacies of ambiguity, including the fallacy of four terms in a categorical syllogism. For example, the word “bat” has at least two meanings: a flying animal, and a piece of sporting equipment (such as a baseball bat or a cricket bat). If these two meanings are not distinguished, the result may be the following categorical syllogism, which is clearly intended as a joke (pun):

1. All bats are animals.
2. Some wooden objects are bats.
3. Therefore, some wooden objects are animals.

Conflating words with different meanings can cause real confusion. For example, respect is used both in the sense of “recognise a right” and “have high regard for”. We can recognise someone’s right to the opinion that humanity is controlled by alien lizards in human form, without holding this idea in high regard. But conflation of these two different concepts leads to the notion that all religious ideas, for example, should be treated with respect, rather than just the right to hold these ideas.

Cartography

In cartography, conflation refers to the act of combining two distinct maps into one new map.
This activity is a special case of image registration.
This can also be performed on imagery or on vector cartographic data (a “digital map”).
Image-to-vector conflation, where an image (such as a satellite image) is modified to match a set of vector data is referred to as “rubbersheeting”.

External links

• Conflations

See

also

• Stemming algorithm
• Portmanteau

Life in the entertainment business

Ortiz began his career as a telenovela actor in Puerto Rico, sharing credits with such actors as Walter Mercado, Alicia Villamil and many others.

He participated in several soap operas of that era.

In 1985, he returned briefly, as a comedian, this time at a show sponsored by Budweiser, at La Taverna Budweiser, alongside Machuchal. Ortiz worked most of his acting career at WAPA-TV.

Apart from his acting career, he was producer of many television shows in Puerto Rico.

Marriages

Elin Ortiz was married briefly to dancer and singer Iris Chacon during the early 1970s. In 1978, he married singer Charytin, a Dominican native who had lived in Puerto Rico for many years. In 1982, they had their first son, Shalim. During the late 1980s, they moved to a mansion in Miami, Florida. In 1991, they had a pair of twins, a boy and a girl. Ortiz has since retired from show business. His son Shalim has gone on to become an international singing star and a spokesman for the American Diabetes Association.

On August 16, 2005, the day that Madonna suffered a horse riding accident, “Escandalo TV”’s castmates decided to play a hoax on their public, saying that Elin Ortiz had suffered a fatal car accident and his wife, Charytin, had been killed. Minutes later, Charytin, visibly surprised, arrived at the show to clarify the rumors.

Ortiz personally suffers from diabetes. He is a spokesperson for various diabetes-related organizations in Puerto Rico and the United States.

Central philosophy

The Orem model is based upon the philosophy that all “patients wish to care for themselves”.

Self care requisites

Self care requisites are groups of needs or requirements that Orem identified. They are classified as either:

• Universal self care requisites - those needs that all people have
• Developmental self care requisites - those needs that relate to development of the individual
• Health deviation requisites - those needs that arise as a result of a patient’s condition

Self care deficits

When an individual is unable to meet their own Self care requisites, a Self Care Deficit occurs. It is the job of the Registered Nurse to determine these deficits, and define a support modality.

Support modalities

Nurses are encouraged to rate their patient’s dependencies or each of the self care deficits on the following scale:

• Total Compensation
• Partial Compensation
• Educative/Supportive

Universal Self Care Requisites (SCRs)

Example nursing assessment

This patient is entirely fictitious and any likeness to any person, alive or dead, is purely coincidental.

‘J’ is a 50-year-old male who has just been diagnosed with type-two diabetes mellitus. He has a history of hypertension, and is a chronic smoker, smoking around 30 cigarettes daily.

• AIR: Educative/Supportive - Provide education on the risks associated with smoking particularly for the diabetic patient.
• WATER: Educative/Supportive - Ensure access to adequate hydration - risk of polydipsia due to hyperglycaemia.
• FOOD: Partial Compensation - Education and provision of a diet that is suitable for his new diagnosis of diabetes, blood sugar monitoring after meals.
• ELIMINATION: Educative/Supportive - May require monitoring.
• ACTIVITY AND REST: Educative/Supportive - Educate patient as to the benefits of cardiovascular exercise, especially for the diabetic
• SOLITUDE AND SOCIAL INTERACTION: Partial Compensation - Nurses may provide social interaction as hospital admission will cause change is social behaviour and interactions.
• HAZARD PREVENTION: Partial Compensation - Nurses will need to educate regarding the medication that he may be taking, and administer this medication initially. Particularly relevant if J is taking insulin injections.
• PROMOTE NORMALITY: Partial Compensation - Nurses will need to facilitate a return to normal lifestyle. This will involve advocating for the patient in a multi-disciplinary team, in order to achieve a medication regime that will fit with the patient’s life.

See also

• Diabetes
• Independent Living
• Dorothea Orem

External links

• The International Orem Society

• Juvenile diabetes is considered an unsatisfactory and somewhat obsolete term because type 1 diabetes can develop in adults, and type 2 can occur in children.
• IDDM includes type 1 diabetes, but as type 2 diabetes progresses, in some people it may reach a degree of insulin deficiency that requires insulin treatment.

See diabetes mellitus, type 1 diabetes mellitus, and type 2 diabetes mellitus.

He was also a founding member of P.A.C.T. (Producers, Actors, Composers and Talents), one of the best known actors’ studios in Sydney. Gordon and Leonard Teale produced “Fill ins” for ABC TV prior to the widespread broadcasting of music videos. His wife Judith died in 1981 and Gordon wrote and directed an episode of A Country Practice in dedication to her and her story. Gordon’s daughter Kerrin-Gai and son Kim both live in Australia.

Piper suffered from diabetes which affected his circulation and eventually resulted in the amputation of both his legs.

The Australian,“Fine bloke on and off TV screen,” 5 October, 2005

References

External links

• Gordon Piper

Derivation

The HOMA authors used data from physiological studies to develop mathematical equations describing glucose regulation as a feedback loop.Turner et al. (1979) Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations. Metabolism 28: 1086–96. They published computer software that solves the equations, so that insulin resistance and beta-cell function can be estimated from fasting glucose and insulin levels. They also published an equation (see below) that gave approximately the same answers as an early version of the computer software.Matthews et al. (1985) Homeostasis model assessment: insulin resistance and B-cell function from fasting plasma glucose and insulin concentrations in man.
Diabetologia 28: 412–9.
The computer model has since been improved to better reflect human physiology and recalibrated to modern insulin assays, and the developers have written that they recommend the computer software be used wherever possible.Wallace et al. (2004) Use and Abuse of HOMA modeling. Diabetes Care 27:1487–95.Levy et al. (1998) Correct Homeostasis Model Assessment (HOMA) Evaluation uses the computer program. Diabetes Care 21: 2191–2.

Notes

The HOMA model was originally designed as a special case of a more general model called HOMA-CIGMA.Turner et al. (1993) Measurement of insulin resistance and beta-cell function: the HOMA and CIGMA approach. Current topics in diabetes research (eds) F. Belfiore, R. Bergman and G. Molinatti Front Diabetes. Basel, Karger 12: 66–75

The approximating equation for insulin resistance, in the early model, used a fasting blood sample, and was derived by use of the insulin-glucose product, divided by a constant:

<math>\frac{\mbox{Glucose} \times \mbox{Insulin}}{405}</math>

where Glucose is given in mg/dL and Insulin is given in μU/mL.

In this equation, one should use the constant 22.5 instead of 405 if the glucose is reported in mmol/L. This model correlated well with estimates using the euglycemic clamp method (r = 0.88).

The authors have tested HOMA extensively against other measures of insulin resistance (or its reciprocal, insulin sensitivity) and beta-cell function. Hermans et al. (1999) Comparison of tests of ß-cell function across a range of glucose tolerance from normal to diabetes. Diabetes 48: 1770–86 Hermans et al. (1999b) Comparison of insulin sensitivity tests across a range of glucose tolerance from normal to diabetes Diabetologia 42: 678–87Wallace et al. (2004) Use and Abuse of HOMA modeling. Diabetes Care 27:1487–95.

References

External links

• http://www.dtu.ox.ac.uk/homa/

History

Fewer than 250 cases of glucagonoma have been described in the literature since their first description by Becker in 1942. Because of its rarity (fewer than one in 20 million worldwide), long-term survival rates are as yet unknown.

Symptoms

The primary physiological effect of glucagonoma is an overproduction of the peptide hormone glucagon, which enhances blood glucose levels through the activation of catabolic processes including gluconeogenesis and lipolysis. Gluconeogenesis produces glucose from protein and amino acid materials; lipolysis is the breakdown of fat. The net result is hyperglucagonemia, decreased blood levels of amino acids (hypoaminoacidemia), anemia, diarrhea, and weight loss of 5-15 kg.

Necrolytic migratory erythema (NME) is a classical symptom observed in patients with glucagonoma and is present in 80% of cases. Associated NME is characterized by the spread of erythematous blisters and swelling across areas subject to greater friction and pressure, including the lower abdomen, buttocks, perineum, and groin.

Diabetes mellitus also frequently results from the insulin and glucagon imbalance that occurs in glucagonoma. Diabetes mellitus is present in 80-90% of cases of glucagonoma, and is exacerbated by preexisting insulin resistance.

Diagnosis

A blood serum glucagon concentration of 1000 pg/mL or greater is indicative of glucagonoma (the normal range is 50-200 pg/mL).

Blood tests may also reveal abnormally low concentrations of amino acids, zinc, and essential fatty acids, which are thought to play a role in the development of NME. Skin biopsies may also be taken to confirm the presence of NME.

A CBC can uncover anemia, which is an abnormally low level of hemoglobin.

The tumor itself may be localized by any number of radiographic modalities, including angiography, CT, MRI, PET, and endoscopic ultrasound. Laparotomy is useful for obtaining histologic samples for analysis and confirmation of the glucagonoma.

Treatment

Heightened glucagon secretion can be treated with the administration of octreotide, a somatostatin analog, which inhibits the release of glucagon. Doxorubicin and streptozotocin have also been used successfully to selectively damage alpha cells of the pancreatic islets. These do not destroy the tumor, but help to minimize progression of symptoms.

The only curative therapy for glucagonoma is surgical resection, where the tumor is removed. Resection has been known to reverse symptoms in some patients.

References

References

• Brewton, John Edmund. Index to Poetry for Children and Young People, 1964-1969. New York: Wilson, 1972.

• Index to Poetry for Children and Young People, 1976-1981. New York: Wilson, 1981.
  

• Sell, Violet, Dorothy B. Frizzell Smith, Ardis Sarff O’Hoyt, and Mildred Bakke. Subject Index to Poetry for Children and Young People. Chicago: American Library Association, 1957.

External links

• http://www.ongoing-tales.com/SERIALS/oldtime/POETRY/

• To help adults who are responsible for administration as well as troop leaders to develop their talents through Scouting to better serve American Indian youth
• To help youth recognize their talents and capabilities through Girl Scouting or Boy Scouting and to serve their communities
• To exchange ideas about successful Girl Scouting and Boy Scouting programs for American Indian youth
• To help youths of all tribes and cultures learn by association to appreciate the wide differences of people of Indian heritage

The AISA began as a committee of concerned Boy Scout scoutmasters in 1956 and was sponsored by the BIA (Bureau of Indian Affairs) in Los Alamos, NM. Its goal was to advise and assist in reaching a maximum number of American Indian youth and leaders with a quality Scouting program. Girl Scout leaders began to participate in 1964, and in 1969, GSUSA assigned a national advisor at the request of Indian participants. The seminars then became a joint venture of Boy Scouts of America and Girl Scouts of the USA in the interest of American Indian youth.

AISA holds an annual seminar, which began in 1957, is run by a volunteer steering committee and is hosted by a local tribe or Indian community designed to attract both Indian and non-Indians to foster understanding of Indian culture and Scouting. Highlights include: parade of traditional clothing, Pow Wow with music and dancing, visit with host tribe, and events/workshops for adults and youth. Youth participation in this seminar began in 1975.

References

• American Indian Scouting Association website
• BSA American Indian Scouting Association website
• Scouting magazine AISA article
• 49th American Indian Boy Scouting/Girl Scouting Seminar

In the past, there was no distinction made between Sheng and Engsh, but the youth speakers of both languages respectively, noticed their inability to understand each other properly. Clearly the languages had evolved differently primarily due to the different economic backgrounds. Nevertheless there are still many similarities between both Sheng and Engsh, but Engsh is unique enough to stand as a language of its own.

Early life

He was the son of Joseph Arnold Himsworth of Huddersfield, West Yorkshire, and he was educated at Spring Grove School and Almondbury Grammar School.

Medical career

He studied medicine at the University of London and trained in University College Hospital (UCH). His early involvement in medical research (especially of diabetes and later of liver disease) would lead to an important 1936 paper in The Lancet, distinguishing the two main types of diabetes.

He was appointed Professor of Medicine at the University of London and the Secretary of the Medical Research Council (MRC) for the very long period of 1949-1968.

He was awarded a knighthood in the New Year honours of 1952 and, in 1953, would be appointed Honorary Physician to the Queen.

His archives are being held by the Wellcome Institute, London.

Sources

• “Sir Harold Himsworth MD FRS (1905–1993)”, Diabetologia Journal, 26 February 2007 (long biography)
• “Huddersfield & District History - Connections With Titled Classes In Modern Times”, Edward Law, 9 April 2002 (short biography)

References

• Himsworth HP. Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types. Lancet 1936;i:127-130.

Life

Viktor Meyer was born in Berlin (1848) as the son of trader and cotton printer Jacques Meyer and Bertha Meyer. His parents were Jewish, though he was not actively raised in the Jewish faith. Later, he was confirmed by the reformed Jewish Church. He married a Christian woman (Hedwig Davidson) and raised his children as such. He entered the gymnasium at the age of ten at the same class as his two year older brother Richard. Although he had excelent science skills his wish to become an actor was based on the love for poetry. At a visit of his brother Ricard, who was studying chemistry at the University of Heidelberg, he became atracted to chemisty.

In 1865, when not even 17 years old but pushed by his parents, Meyer began studying chemistry at the University of Berlin, the same year that August Wilhelm von Hofmann succeeded Eilhard Mitscherlich as the chair of chemistry there. After one semester, Meyer went to Heidelberg to work under Robert Bunsen, there also hearing lectures on organic chemistry by Emil Erlenmeyer. As no research was required under Bunsen at the time, Meyer received his doctorate in 1867, at the age of nineteen. This opened the doors to a very successful career in which he became one of the most important chemists of his time. He stayed one year with Bunsen for an area wide analysis of spring water. Besides this he was also able to teach some PhD students. He joined the group of Adolf Baeyer, one of his best friends in later life, in Berlin changing from inorganic chemistry to organic chemistry. At the age of 23 Baeyer sent him to Stuttgart at a request from Fehling for a student capable to be a lecturer at the University.

Overworked and overtaxed, Meyer’s nervous system suffered, leading to several minor and major nervous breakdowns during the last years of his life. He always failed to recover completely, yet continued working. He took pills to fall asleep, but these had a damaging effect on his nervous system. In one of his depressions, Meyer decided to take his own life, and committed suicide by taking cyanide. He died at the age of forty-nine during the night of August 7 - August 8 1897 in Heidelberg. It was a shock to others as Meyer was considered a highly gifted scientist by his colleagues, and a very talented teacher by his students.

Career

Meyer’s professional career:

Scientific contributions:

• Synthesis of aromatic carboxylic acids from sulfonic acid and formiates (1869).
• Nitroalkanes from alkyl iodides and silver nitrite (1872).
• Development of a method to distinguish primary, secondary and tertiary nitroalkanes (1875).
• Starting with studying physical chemistry in 1876, Meyer created a new method for determining gas density in 1878. This method allowed him to demonstrate how arsenious oxide vapours corresponded to the formula As₄O₆, that mercury, zinc and cadmium yielded monatomic vapours, and that halogen molecules dissociated into atoms on heating, a phenomenon which he studied until his death. The Victor Meyer apparatus accurately measures the volume of a volatilized substance from which the vapor density of the gas can be derived and also the relative mass.
• Proposing glucose is an aldehyde and not a ketone, hereby correcting von Baeyer and van’t Hoff (1880).
• Synthesis of aldoximes and ketoximes from hydroxylamine and aldehydes or ketones, hereby discovering a new structural identification and elucidation method (1882, together with Alois Janny).
• Identification of thiophene as a contaminant in benzene derived from coal (1882). Benzene produced by decarboxylation of benzoic acid did not contain this impurity.
• First reliable synthesis of pure sulfur mustard (1886, also see Meyer’s account on sulfur mustard)
• Coining of the concepts of stereochemistry and dipole in 1888. Meyer had always been interested in stereochemical problems and was one of the first ones to instruct his pupils with van’t Hoff’s theory of asymmetric carbon and the Hantzsch-Werner theory.
• Discovery of iodoso compounds in 1892 by reacting o-iodobenzoic acid with nitric acid.
• Observation (1892) that ortho-substituted benzoic acid derivatives are esterified with difficulty. This principle is now known as the Victor Meyer esterification law and was discovered in an attempt to esterify o-iodosobenzoic acid.
• Discovery of iodonium compounds by reacting iodobenzene and iodosobenzene (1894).

Books:

Meyer wrote several notable books:

• Tabellen zur qualitativen Analyse (1884, written together with Frederick Treadwell)
• Pyrochemische Untersuchungen (1885)
• Die Thiophengruppe (1888)
• Chemische Probleme der Gegenwart (1890)
• Ergebnisse und Ziele der Stereochemischen Forschung (1890)
• Lehrbuch der organischen Chemie (1893, written together with Paul Jacobson. A very popular book at the time that has been reprinted and reedited several times)
• Märztage im kanarischen Archipel, ein Ferienausflug nach Teneriffa und Las Palmas (1893, travel guide)

See also

• Victor Meyer apparatus: In a demonstration in Cohen’s Practical Organic Chemistry (1910) the molar mass of diethyl ether was determined experimentally at 72 g/mol and that for aniline 93 g/mol.

Further reading

• Richard Meyer. Victor Meyer. Leben und Wirken eines deutschen Chemikers und Naturforschers,1848-1897 (Akademische Verlagsgesellschaft, 1917) (note: Richard Meyer is Victor Meyer’s brother).

References

• W Pötsch. Lexikon bedeutender Chemiker (VEB Bibliographisches Institut Leipzig, 1989) ISBN 3-8171-1055-3)
• E von Lippmann. Zeittafeln zur Geschichte der organischen Chemie (Julius Springer, 1921)
• G Bugge. Das Buch der grossen Chemiker (Verlag Chemie GmbH, 1955)

The court also has authority to allow minors, under certain circumstances, to seek abortions. It may also emancipate a child.

References

The Juvenile and Domestic Relations District Court.

Its objective is to conduct independent research to contribute to the resolution of contemporary complex social issues in many areas, including politics, economics, international affairs, society, new technologies, and administration.

It maintains a World Directory of Think Tanks.

See also

• Home page

The most common glucocorticoids which cause steroid diabetes are prednisone and dexamethasone given systemically in “pharmacologic doses” for days or weeks. Typical medical conditions in which steroid diabetes arises during high-dose glucocorticoid treatment include severe asthma, organ transplantation, cystic fibrosis, inflammatory bowel disease, and induction chemotherapy for leukemia or other cancers.

Glucocorticoids oppose insulin action and stimulate gluconeogenesis, especially in the liver, resulting in a net increase in hepatic glucose output. Most people can produce enough extra insulin to compensate for this effect and maintain normal glucose levels, but those who cannot develop steroid diabetes.

The diagnostic criteria for steroid diabetes are those of diabetes (fasting glucoses persistently above 125 mg/dl (7 mM) or random levels above 200 mg/dl (11 mM)) occurring in the context of high-dose glucocorticoid therapy. Insulin levels are usually detectable, and sometimes elevated, but inadequate to control the glucose. In extreme cases the hyperglycemia may be severe enough to cause nonketotic hyperosmolar coma.

Treatment depends on the severity of the hyperglycemia and the estimated duration of the steroid treatment. Mild hyperglycemia in an immunocompetent patient may not require treatment if the steroids will be discontinued in a week or two. Moderate hyperglycemia carries an increased risk of infection, especially fungal, and especially in people with other risk factors such as immunocompromise or central intravenous lines. Insulin is the most common treatment.

Steroid diabetes must be distinguished from stress hyperglycemia, hyperglyemia due to excessive intravenous glucose, or new-onset diabetes of another type. Because it is not unusual for steroid treatment to precipitate type 1 or type 2 diabetes in a person who is already in the process of developing it, it is not always possible to determine whether apparent steroid diabetes will be permanent or will go away when the steroids are finished. More commonly undiagnosed cases of type 2 diabetes are brought to clinical attention with corticosteroid treatment because subclinical hyperglycemia worsens and becomes symptomatic. Generally, steroid diabetes without preexisting type 2 diabetes will resolve upon termination of corticosteroid administration.

Steroid diabetes does not occur with other steroid hormones, such as anabolic steroids, mineralocorticoid, or sex steroids because these other categories of steroids have little effect on glucose metabolism.

Hyperinsulinism due to diminished sensitivity, associated with diabetes risk

Although many factors influence insulin secretion, the most important control is the amount of glucose moving from the blood into the beta cells of the pancreas. In healthy people, even small rises in blood glucose result in increased insulin secretion. As long as the pancreatic beta cells are able to sense the glucose level and produce insulin, the amount of insulin secreted is usually the amount required to maintain a fasting blood glucose between 70 and 100 mg/dL (3.9-5.6 mmol/L) and a non-fasting glucose level below 140 mg/dL (<7.8 mmol/L).

When liver cells and others that remove glucose from the blood become less sensitive and more resistant to the insulin, the pancreas increases secretion and the level of insulin in the blood rises. This increased secretion can compensate for reduced sensitivity for many years, with maintenance of normal glucose levels. However, if insulin resistance worsens or insulin secretion ability declines, the glucose levels will begin to rise. Persistent elevation of glucose levels is termed diabetes mellitus.

Typical fasting insulin levels found in this type of hyperinsulinism are above 20 μU/mL. When resistance is severe, levels can exceed 100 μU/mL.

In addition to being a risk factor for type 2 diabetes, hyperinsulinism due to insulin resistance may increase blood pressure and contribute to hypertension by direct action on vascular endothelial cells (the cells lining blood vessels). Hyperinsulinism has also been implicated as a contributing factor in the excessive production of androgens in polycystic ovary syndrome.

The principal treatments of hyperinsulinism due to insulin resistance are measures that improve insulin sensitivity, such as weight loss, physical exercise, and drugs such as thiazolidinediones or metformin.

Hyperinsulinism due to inappropriate secretion, associated with hypoglycemia

Hyperinsulinism is also used in medical contexts to refer to forms of hypoglycemia caused by excessive insulin secretion. In normal children and adults, insulin secretion should be minimal when blood glucose levels fall below 70 mg/dL (3.9 mM). There are many forms of hyperinsulinemic hypoglycemia caused by various types of insulin excess. Some of those that occur in infants and young children are termed congenital hyperinsulinism. In adults, severe hyperinsulinemic hypoglycemia is often due to an insulinoma, an insulin-secreting tumor of the pancreas.

Insulin levels above 3 μU/mL are inappropriate when the glucose level is below 50 mg/dL (2.8 mM), and may indicate hyperinsulinism as the cause of the hypoglycemia. The treatment of this form of hyperinsulinism depends on the cause and the severity of the hyperinsulinism, and may include surgical removal of the source of insulin, or a drug such as diazoxide or octreotide that reduces insulin secretion.

Dr. Seale Harris first diagnosed hyperinsulinism in 1924 and also is credited with the recognition of spontaneous hypoglycemia.

Hyperinsulinism due to insulin injection

The treatment of diabetes mellitus with insulin replacement therapy can easily result in diabetic hypoglycemia due to the difficulty of balancing insulin delivery.

Transient hyperinsulinism can also occur when insulin is injected by non-diabetic athletes attempting to enhance their anaerobic performance.

References

OneTouch Ultra Blood Glucose Meters provide blood glucose test results in 5 seconds, offer alternate test site options, and various memory and flagging features.

OneTouch Meters are sold in kits containing a carry case, a lancing device, control solution, sample quantities of lancets, and a replacement cap for use with the sampling device when using alternate site testing.

The OneTouch Ultra 2 is similar in design and operation to the OneTouch Ultra Meter, but also offers Before and After Meal Flags, Comments, and a list style memory recall. This meter also provides 7 day, 14 day, and 30-day averages, with the option of averaging Before meal or After Meal records.

Other OneTouch Ultra Meters include the OneTouch UltraSmart and the OneTouch UltraMini Meter (known as the OneTouch UltraEasy in Europe). In addition to the original Silver Moon color, LifeScan introduced three additional colors of the OneTouch UltraMini Meter in summer 2007: Pink Glow, Limelight, and Jet Black.

OneTouch Meters with data ports can be used in combination with the downloadable OneTouch Diabetes Management Software and a PC to compute averages and trends. The software is available from LifeScan’s Web site but an interface cable must be purchased.

Notable ad campaigns

• B.B. King has had diabetes for 10+ years. He was in an ad campaign for OneTouch Ultra, describing how blue he feels from diabetes. There was also a commercial with him and a younger person with diabetes who also played blues music. The campaign promoted the use of alternate site testing.
• Patti Labelle has had diabetes for 12+ years. She was in an ad campaign for OneTouch Ultra2, describing how she collapsed on stage and discovered she had diabetes. Labelle re-recorded her 80’s hit New Attitude (Patti Labelle song) for one of the commercials.
• OneTouch is also the main shirt sponsor of Inverness Caledonian Thistle, highlighting LifeScan’s presence as a major employer in the city.

See also

• LifeScan
• Animas Corporation

References

• OneTouch Meters
• OneTouch UltraMini Meter
• OneTouch Ultra2 Meter
• OneTouch Ultra Meter