text:
Handbook of Genetic Counseling/Cerebral Palsy

Cerebral palsy

Contracting

 * What is your understanding of why you were referred to genetics?
 * What questions or concerns would you like us to address today?
 * Set agenda for the session

Etiology

 * Heterogeneous group of conditions usually leading to ataxia
 * Sometimes inherited in autosomal dominant, autosomal recessive, or X-linked form in familial cerebellar hypoplasia

 * Congenital and childhood-onset ataxias tend to be autosomal recessive
 * Adult-onset conditions tend to be autosomal dominant
 * May also be due to teratogenic insults
 * Methymercury
 * Retinoic acid
 * Anticonvulsants
 * Most common cause is hypoxic/ischemic injury in perinatal period or early childhood
 * Anoxia
 * Trauma to the brain at birth
 * Can be caused by cerebral injury later in life

Clinical Features

 * Several classes with different features
 * Spastic diplegia
 * Onset several weeks or months after birth
 * Delay in normal development, especially motor skills
 * Results from prenatal or perinatal insult
 * Walking attempted much later and results in characteristic stance and gait
 * Legs advanced stiffly in short steps like arc of circle
 * May have scissors gait with crossing over of legs
 * Lower legs splayed out, feet flexed and turned in, heels not touching ground
 * Posture alternates between extremes of supination and pronation
 * Walking accompanied often by rotary movements of neck and facial grimacing
 * Legs short and small but muscles not atrophic
 * Arms may also be mildly affected
 * Hemiplegia
 * Difference in function of right and left extremities noticed after birth or 6-12 months
 * Accounts for about 1/3 of children with cerebral palsy
 * Affects arms first, noticed in legs when learning to walk
 * Mental defects depend on whether brain lesion confined to one hemisphere
 * Convulsions (35-50%)
 * Seizures may accompany onset if develops during childhood
 * Usually limited to hemiplegic side of body
 * May persist throughout life
 * Double hemiplegia
 * Occurs less frequently than hemiplegia
 * Bilateral weakness of face, arms, and legs
 * Begins at any age due to acquired cerebral disease
 * May be due to bilateral cerebral lesion or high cervical cord lesion
 * May also be produced in infant by fracture-dislocation of cervical spine by breech delivery
 * Arms severely affected
 * Congenital choreoathetosis
 * Recognized after several months or a year
 * Causes some combination of chorea, athetosis, ballismus, myoclonus, and dystonia
 * Causes defect in voluntary movement
 * May be mild resulting in "fidgets"
 * May be severe, intense involuntary movements
 * Even with rehabilitation, the most severe rarely achieve enough motor control to live independent life
 * Intelligence may not be affected
 * Kernicterus
 * Was common when postnatal serum bilirubin was kept below 15 mg/dL
 * Majority of infants die within 1 or 2 years
 * Survivors usually mentally retarded, deaf, and totally unable to sit, stand, or walk
 * Several patients reportedly were not mentally retarded and learned to walk backwards
 * Have rigid limbs

Management/Treatment Options

 * Outcome depends on severity of associated intellectual handicaps
 * Early application of stretching to prevent contractures
 * Orthopedic appliances and surgical procedures to improve mobility
 * Special education to help with motor problems and intellectual involvement
 * Prevention is great challenge
 * Prevention of kernicterus by phototherapy has helped
 * Providing low-birth weight infants with extra care may help
 * More prone to respiratory distress
 * Must provide good surveillance of respiratory function

Differential Diagnosis

 * Leukodystrophy - spinal tap showing elevated spinal fluid indicates leukodystrophy
 * Hydrocephaly if child has large head
 * Tumor of cerebral hemisphere - disease is progressive
 * Spinal cord lesions - weakness limited to lower extremities
 * Muscular dystrophy - tendon reflexes would be normal
 * Ataxia telangiectasia

Recurrence Risks

 * Depends if cause of cerebral palsy can be determined
 * Autosomal recessive
 * Each pregnancy from heterozygote parents has 25% risk of child being affected
 * Each pregnancy has 50% risk of being carrier
 * Autosomal dominant
 * Each child born to affected parent has 50% chance of being affected
 * May also occur due to new mutation so low recurrence risk
 * X-linked
 * Sons of affected males not affected
 * Daughters of affected males must be affected
 * Daughters of carrier females 50% risk of being carriers
 * Sons of carrier females 50% risk of being affected
 * Most cases probably caused by hypoxic or ischemic injury to brain so recurrence risk is low

Psychosocial Issues

 * Parental guilt
 * Burden of disease that requires daily management
 * Social stigma
 * Financial pressures, disruption of daily activities for special therapies, orthotics, or other needs
 * Potential need for lifetime care


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Clarinet/General

Getting to Know the Clarinet
The clarinet has six different parts to it:

as illustrated in the diagram.
 * Mouth piece
 * Ligature
 * Barrel Joint
 * Upper Joint
 * Lower Joint
 * Bell

A clarinet cannot play unless you have a reed, which is held onto the mouthpiece by the ligature. The reed vibrates at a very high speed (changes with each note, but remains at a high rate no matter what) when the player blows through the clarinet which in turn makes sound.

Getting Started
Now that we know the different parts of the clarinet, let's get started. As clarinetists, we will need to get the tools necessary to keep the clarinet clean and in working order. The following "tools" are what the most prestigious of players use to keep their instrument, the clarinet, in top working order:

 * Polishing cloth.
 * Old cloth.
 * Cork grease.
 * Swab. (the best candidate is a handkerchief tied to a thick string, or a swab that can be purchased at almost any music store).

So now that we have our "tools", let's put together the clarinet:

 * 1) Moisten the reed in your mouth. You may want to run it under some water if your mouth is dry.
 * 2) If necessary, put a small amount of cork grease on the ends of the clarinet that has a cork stub.  It should just be enough to make the cork a little slippery, Do not put an excess amount of cork grease on the cork of the clarinet. Greasing the Corks is only needed when you find it hard to put the Clarinet Pieces together. If the grease does not improve it, you may need to replace your corks.
 * 3) Now take the bottom of the bell and place it in the palm of your right hand and clasp your fingers around it.
 * 4) Now take the lower joint in your left hand, be sure that the thumb rest is in the creves between your thumb and index finger and clasp your fingers around the keys of the lower joint.
 * 5) Now put the two ends together being sure to twist back and forth until they are secure and you cannot push them together anymore
 * 6) Now with your right hand take hold of the bell while placing your thumb on the last pad on the lowest part of the clarinet, and with your left hand take a hold of the upper joint similar to the way you did with the lower joint in step 3, but this time there will be no thumb rest. Make sure that the bridge key on each of the two main joints line up perfectly and touch. This is essential for the clarinet to work properly.
 * 7) Now twist the two joints together in a back and forth motion, be sure that the lever on the side that was mentioned in step 8 and the lever on the same side of the lower joint are aligned.
 * 8) Now put the barrel joint on, then the mouth piece and ligature on in that order. Do not put the ligature on too tightly, but merely turn the screws until it is snug. Turning the ligature screws too tightly inhibits proper reed vibration, producing an unsatisfactory tone.  Over-tightening to extreme levels can destroy the reed or even the mouthpiece.
 * 9) Now put the reed on the mouth piece, be sure that the reed is placed evenly on the table of the mouth piece and that when you push on cut of the reed the tip is black because it touches the tip of the mouth piece, placing the reed on the clarinet correctly might take a little practice before one gets the hang of it.

All of these procedures are necessary to keep the clarinet in good working order. The number of instruments sent in to be repaired could be decreased by about 70% if they were assembled correctly.

Kларинет/Делови

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

title: Clarinet/General


text:
Clarinet/Clarinet Basics/Tone

Tone
Tone is usually made up of two parts, airflow and embouchure. There is still the matter of deciding your mouthpiece/reed combination that best suits you, but the player doesn't need that until he or she can establish good airflow, and a good embouchure. The tone of the clarinet has made it famous. Before the clarinet and even today there isn't an instrument with the dark and fluid sound of a clarinet. The tone of a clarinet depends nearly solely on what's going on at the top of the clarinet, i.e. is there a steady airstream going through the clarinet? Is the embouchure set correctly? Is there a good reed that's compatible with the mouthpiece and the player? Does the mouthpiece suit the player well? All of these questions are questions to ask when trying to create a good tone on the clarinet.

Kларинет/Toн

title: Clarinet/Clarinet Basics/Tone


text:
Handbook of Genetic Counseling/CHARGE Association

CHARGE Syndrome

Contracting

 * Find out what your concerns are
 * Review family history
 * Review medical history
 * Physical exam
 * Recommend testing options
 * Answer any questions

Additional psychosocial Issues

 * Having to learn a lot in a short amount of time
 * Support system? The difficulty of raising three kids on your own with one having medical dependence.
 * Coping strategies
 * Does she have a home care nurse?
 * Has she used respite care, does she know about it?

Possible counseling issues - CHARGE Syndrome

 * Autosomal dominant, most often de novo pathogenic variants in CHD7 gene on chromosome 8
 * Recurrence risk for next child = 1-2%
 * Resources for parents: see New Parent Packet at www.chargesyndrome.org
 * See fact sheet below for more details that may need to be addressed

What Is It?

 * A specific set of birth defects that are found in a single child. The letters of CHARGE are no longer used for diagnosis. Diagnosis is by major and supporting features
 * Major features
 * Coloboma in 80-90% (a cleft in the eyeball: iris, retina or disc)
 * Choanal atresia in 50% - (blockage or narrowing of the passageway that connects the nose to the throat and allows a person to breathe through their nose. Extremely dangerous because newborns are obligate nose breathers until 4-6 weeks old.)
 * C- cranial nerve anomalies (nearly everyone has at least one)
 * CN I - olfactory 80% (decreased or absent sense of smell)
 * CN VII - facial palsy 40% (one or both sides)
 * CN VIII - sensorineural hearing loss 90%
 * CN IX, X - swallowing difficulties (70%)
 * Characteristic external ear shape
 * Characteristic inner ears on MRI
 * fewer turns to the cochlea
 * small or absent semicircular canals 95%
 * Supporting features
 * Heart defect in 70-85% (usually a VSD, PDA, Tetralogy of Fallot, or DORV - double outlet right ventricle)
 * Genitourinary anomalies in 70-80% of males (small penis, hypospadias, undescended testicles)
 * Kidney abnormalities
 * Cleft lip
 * Tracheal or esophageal abnormalities
 * Post-natal short stature, sometimes with growth hormone deficiency

What Are Other Manifestations?

 * Feeding problems are common/swallowing difficulties
 * Developmental delay in 100% - because of multiple hospitalizations and sensory deficits (hearing, vision, balance)
 * Intellectual ability - from normal to profoundly impaired. About 50% have normal intelligence
 * Visual impairment
 * Characteristic facial features in >50% (square face, large eyes, small nostrils, small mouth, facial asymmetry with or without paralysis)
 * Usually there is not growth retardation prenatally. Typically babies are born with an average weight and then linear growth starts to shift below the third percentile by 6 months of age.
 * Typical behaviors may look similar to autism but are likely not autism

What Is the Cause?

 * The diagnosis is clinical, based on features. All suspected children should get gene testing
 * The only known cause for CHARGE syndrome are pathogenic variants (mutations) in the CHD7 gene on chromosome 8. 10-20% of children with clinical diagnosis have negative (normal) CHD7 testing
 * Most of the time, the child with CHARGE is the first in the family to have it (de novo)

What Is the Incidence?

 * 1/10,000 - 1/12,000 births

What Is the Recurrence Risk?

 * Recurrence of an affected sibling with two unaffected parents = 1-2%
 * An adult with CHARGE has a 50% chance of passing the gene on to each child. If a child inherits the CHD7 variant, that child may have features somewhat different from the parent.

What Is the Predicted Outcome?

 * Mortality
 * There is a high mortality in children with CHARGE in the first three years - due to severe birth defects, multiple hospitalizations and surgeries. Many have severe breathing problems and/or difficulty with anesthesia
 * After the first three years, children with CHARGE remain medical fragile and have higher morbidity and mortality than typical children. Even as adults, there is a higher risk of death, most likely related to breathing and swallowing issues.
 * Motor milestones
 * Motor development will be delayed due to birth defects, surgeries, illness, low upper body tone, very poor balance (due to abnormal semicircular canals), low vision and poor hearing. Although delayed, children with CHARGE will eventually reach all milestones
 * Language will be delayed due to hearing loss and other issues, especially vision loss. Hearing should be tested and augmented as soon as possible.  Deafblind educators (those with skills to deal with children with combined decreased vision and hearing) should be involved from early on.

What Are the Management Suggestions?

 * Ophthalmology exam
 * Cardiac evaluation
 * Kidney ultrasound
 * Hearing Test
 * ENT evaluations, often with pulmonary because of breathing issues
 * MRI of inner ear to evaluate middle and inner ear structures
 * Placement of stents (plastic tubes) in the nasal passageway.
 * Placement of a G-tube for feeding if reflux is severe.
 * Endocrinology evaluation by age 3 years

Is Prenatal Testing Available?

 * If a family has one child with a known CHD7 variant, prenatal diagnosis by genetic analysis (CVS, amniocentesis) is possible
 * Ultrasound can evaluate for some features common in pregnancies where the fetus has CHARGE:
 * Polyhydramnios
 * Cardiac involvement
 * Genitalia
 * Kidneys
 * Cleft lip/palate
 * Characteristic ears by 3D ultrasound

What Are Resources for Parents?

 * CHARGE Syndrome Foundation, Inc: A better world for people with CHARGE syndrome. The CHARGE Syndrome Foundation champions the lifelong potential of people with CHARGE syndrome through outreach, education and research.
 * www.chargesyndrome.org   1-800-442-7604
 * see especially New Parent Packet, For Families, and Resources
 *

 * CHARGE Syndrome. Ed. Hartshorne, Hefner, Davenport, Thelin
 * https://www.pluralpublishing.com/publication_cs2.htm


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Handbook of Genetic Counseling/Chondrodysplasia Punctata

Chondrodysplasia Punctata (X-linked Dominant - Conradi-Hunermann)

Introduction

 * Assess concerns and ask what they hope to gain from the session
 * Discuss reason for follow-up
 * Provide overview of session
 * Interim medical/developmental history
 * Discussion of concerns/questions
 * Dr. will come in and do physical exam
 * Discussion about follow-up plans

Elicit interim medical history

 * Any illnesses/hospitalizations/surgeries since last visit in
 * Current medications-are there any?
 * Any recent medical tests or procedures?
 * Immunizations up to date?
 * Review of systems

Psychosocial update?

 * Any changes in work?
 * Any changes with who is around at home?
 * How are things around the home generally?

Genetic etiology

 * Several forms of chondrodysplasia punctata known-about 25% of these are of the X-linked dominant type
 * Incidence figures are difficult to determine because it is very rare
 * ____'s is likely due to a new mutation, although there is some chance one of the parent's has gonadal mosaicism
 * Recurrence risk for parents to have another child with _____'s condition is probably less than 2% (probably MUCH less, but in case of gonadal mosaicism, we should say this number)
 * Risk for _____to have a child with her condition: 33% affected female, 33% unaffected female, 33% unaffected male (affected males usually die from condition in utero)

Molecular genetics

 * Exact gene associated with this condition is unknown
 * People with this condition have been found to have mutations in Δ8-Δ7 sterol isomerase, an enzyme involved in the biochemical pathway leading to the synthesis of cholesterol
 * People with this condition typically have elevated levels of 8(9) cholestanol, a product in the pathway of cholesterol synthesis

Testing options

 * Testing serum 8(9) cholestanol levels is a highly sensitive way of detecting people with the sterol isomerase mutation
 * Clinical and research testing is available for both the serum 8(9) cholestanol level analysis and mutation analysis at several sites throughout the country
 * There are research trials underway to understand the spectrum of mutations in the sterol isomerase gene

Support groups

 * MUMS: National Parent to Parent Network
 * Julie J. Gordon
 * 150 Custer Court
 * Green Bay, Wisconsin 54301-1243
 * 1-877-336-5333 (Parents only please)
 * 920-336-5333
 * 1-920-339-0995 (fax)
 * E-mail: mums@netnet.net
 * [Web: http://www.netnet.net/mums]
 * This is a great organization. Can hook up parents of children with a particular condition with a family that has a child with that same condition. There are 4 people registered on this network with this condition. This can be helpful if the parents really want to know what to expect. This will not be so helpful if they are paired with a family whose child has had a much better or much worse time with the condition. It could give false hope, or more likely could make the family feel more afraid of what is to come. Should only be offered to parents who really seem to have a lot of questions about what to expect in the future.

Resources

 * Smith's Recognizable Patterns of Human Malformation
 * OMIM-entry # 302960


text: Template:Non-free software screenshot

title: Template:Non-free software screenshot


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User talk:71.111.168.96

Please stop adding nonsense to Wikibooks. It is considered vandalism. If you would like to experiment, use the sandbox. Thank you.

title: User talk:71.111.168.96


text:
User talk:59.163.146.6

Please stop. If you continue to blank pages, you will be blocked from editing.

title: User talk:59.163.146.6


text:
User talk:70.26.56.242

Teaching our children well: your concerns about white supremacism and racism in my writing about Venezuela

 * Hello!
 * Thank you for your edits to the WikiJunior page on Venezuela, which I have only just seen.
 * I must admit I don't know much about the problems of racism/white supremacism over there. And indeed in all of South America.
 * (Really I cannot comment on Poles and racism or otherwise, or rather, I do not wish to).
 * I do appreciate how hard it must be for people (like me) to write about the place when they don't live there or even know there.
 * When I said 'civilians' I certainly never meant for them to have any colour or race. I only meant people who weren't military.
 * And surely a leader is elected for what he or she means to the people. I wasn't fully aware of what the businessmen did to Chavez, though I may have suspected as much in media coverage which I have read over the years. And if he were recalled from office, well, that puts a different complexion (sorry about the pun) on things.
 * I agree I was loading the dice slightly by putting European first, then African, then indigenious. Too broad a brush, perhaps. And if it wasn't accurate...
 * Well, ignorance is most certainly not an excuse, particularly where children are involved/concerned. Ethnicity is not really such an obvious thing; not in words anyway.
 * I greatly appreciate your edits on Venezuela and the rest of WikiJunior South America, and I appreciate your concern. It's not exactly right to have the whole world read about it.
 * I realise I have a lot to learn and I hope I will continue to learn. And I will learn to read my sources more critically and interpret them more accurately. Particularly first-hand ones!
 * Here, by the way, are my sources:

[|Venezuela] and [|Demographics of Venezuela]. --EuropracBHIT 09:42, 17 November 2005 (UTC).

title: User talk:70.26.56.242


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User:Stevy76~enwikibooks

{|width="100%"
 * style="vertical-align:top" |
 * style="vertical-align:top" |

Über mich / About me
siehe: Wikipedia/Benutzer:Stevy76

see here: Wikipedia/User:Stevy76 (german)

 * }
 * }

de:Benutzer:Stevy76

title: User:Stevy76~enwikibooks


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Talk:General Biology/Classification of Living Things/Eukaryotes/Animals/Chordates

Page http://en.wikibooks.org/wiki/Chordates_(General_Biology) needs complete revision as it has many defects ranging from spelling errors (e.g. "natho-stomes") to serious misclassifications (e.g. entries for "synapsid" and "pelycosaur" under "diapsid"!).

Some other suggestions:
 * It's difficult to squeeze the whole of chordate or vertebrate phylogeny into 1 page. It might be best to adopt the compact style used by e.g. Palaeos (http://www.palaeos.com/Vertebrates/Lists/Cladograms/100Summary.html), an dmake the names in the tree link to descriptions either further down the page (need to be brief) or in other pages.
 * Deciding the structure of the page(s) about chordates (or any other high-level taxon) needs centralised editorial control in order to make sure the structure is coherent, e.g. whether to have descriptions in the same page as the outline phylogenetic tree or on separate pages or both.
 * High-level phylogeny pages must acknowledge that some areas of the tree are under debate and therefore fluid, e.g. synapsids, whether monotremes are actually in the same "branch" as marsupials and placentals, early hominid evolution.


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How to Write a Research Paper in History/Citing your sources

The most important part of citing your sources is following your teachers' instructions and obtaining a copy of the correct style manual in its current edition. Style manuals vary widely amongst themselves and between editions. For example, the American Psychological Association made major revisions in citation style between the fourth and fifth editions. Do not assume that teachers in the same school use the same style manual. If in doubt, ask early in the writing process.

Learning a citation style well can be very useful, at least in a few standard forms. Memorizing the format for books and journal articles, for example, will probably mean you will not have to consult your style guide for the vast majority of your citations. This will save time (and misery) and allow you to concentrate more on the actual writing of the paper than on the formalistic aspects of citation.

Citation itself is very important for two major reasons. First is that citation allows you to give adequate credit to what others have said — this is important in order to ward off plagiarism and all of its evils, and is additionally valuable because "credit" is one of the primary currencies of academia (even if you don't regard it as such, your professor probably will).

Citation also allows the reader to know where your sources are located and what sources you have consulted—useful to your paper graders both in assessing both your argument as well as how much work you have done, and necessary in general to appreciate the value of a historical paper.

How to Cite
In-text citations: Author’s last name, year, page number(s) if applicable. For subsequent citations of the same source use the same format as the first.

References list: At the end of your paper include a full list of all sources cited. Author(s), title, date, publisher and place of publication (for books), journal name, volume, issue, page numbers (for articles), and any other relevant details.

Next section: ../Additional resources/


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User:Kalinyaprak~enwikibooks

See E-Learning How-To..

Wikilearning...

Hakan KALINYAPRAK, MSc., PhD. candidate,

Vienna University of Technology;

Institute for Software Technology and Interactive Systems

Favoritenstrasse 9-11/188-1, A-1040 Wien

WWW: http://www.ifs.tuwien.ac.at/hakan

Projects: TELFI - Telelernen für HaftinsassInnen - (E-Learning for imprisoned people) and Step by Step

title: User:Kalinyaprak~enwikibooks


text:
Operating System Design/Command line interfaces

A command line interface or CLI is a method of interacting with a computer by giving it lines of textual commands (that is, a sequence of characters) either from keyboard input or from a script. They were originally developed for interfacing with computers over teletype machines in the 1950s. It is occasionally also referred to as a CLUE, for Command Line User Environment. Some argue that the CLI is not actually a user interface at all, but a programming language, entered one line at a time, and has very little utility for users compared to developers. Indeed, command lines are most often used in scientific or engineering environments for programming.

In its simplest form, the computer displays a prompt, the user types a command on the keyboard and terminates the command with a keyboard key (usually the Enter key) and the computer executes the command. The computer then carries out the command given. The term is usually used in contrast to a graphical user interface (GUI) in which commands are typically issued by moving a pointer (via a pointing device) to a zone of the screen and pressing a button mounted on the pointing device (clicking).

Programs that implement these interfaces are often called command line interpreters. Examples of such programs include the various different Unix shells, VMS' DCL (Digital Command Language), and related designs like CP/M and DOS's command.com, both based heavily on DEC's RSX and RSTS operating system interfaces (which were also command line interfaces). Microsoft claims their next major operating system, Windows Vista, will include an enhanced command line interface named MSH (Microsoft Shell, codename Monad), which combines the features of traditional Unix shells with the object-oriented .NET framework.

Some applications provide command lines as well. The CAD program AutoCAD is a prominent example. Another excellent example is the engineering/scientific numerical computation package Matlab, in which practically no GUI exists and/or is unnecessary for performing most of the calculations. In some computing environments like the Oberon or Smalltalk user interface, most of the text which appears on the screen may be used for giving commands. The commands given on a command line interface are often of the form

[doSomething] [how] [toAFile]

or

[doSomething] [how] < [inputFile] > [outputFile]

doSomething corresponds to a verb, how to an adverb (it describes how the command should be performed in this instance — for example, should it be particularly "verbose", or particularly "quiet") and toAFile to an object (often one or more files) against which the command should be run. The standalone '>' in the second example is a redirection character, telling the operating system (i.e., usually a command shell interpreter) to send the output of the previous commands (that is, those on the left of '>') to some other place (that is, the file named to the right of the '>'). Another common and important redirection character is the pipe ('|'), which tells the CLI to treat the output of this command as the input of another; this can be a very powerful mechanism for the user, as explained under pipeline (Unix) and pipes and filters.


text:
Talk:Handbook of Genetic Counseling

How Can You Contribute?
If you are a genetic counselor/consultant/clinical geneticist visiting this site and using these outlines in your own practice, please considering updating the content of this book by supplementing the information with your own research findings.

Other ways in which you can contribute:
 * Clean up the outlining
 * Fix hyperlinks or add links to Wikipedia or other online resources
 * Add new outlines for conditions that have not been included in this text
 * Update Wikipedia articles on these conditions - it will improve Wikipedia and help you learn more about the condition at the same time

MIM numbers
Think it would be better, that each disease would have own MIM number with the link to OMIM in the headnote - already started add or transfer them from references. Ramujana 1 Dec, 2005
 * Seems like a good idea. Maybe once I finish transferring all of the outlines over I'll start on that.

Copyright Issues
This Handbook seems to be a Copy from, and it might be a legal copy but do not state the source nor if it is a legal copy. Also ref Copyright notice on bottom of. Have not put it on CopyVio-list as I'm not shure it is... Oyvind 12:31, 17 November 2005 (UTC)
 * That site is being taken down. It did not have enough people contributing to it because of the CMS software that was being used.  As soon as all of the outlines from that site are transferred to here, that site will be taken down.  My wife is the person who set up the other site (with my help) so she holds the "copyright" on that other site.  She is happy to move the outlines here hoping other people will contribute to them given how easy it is to do so on Wikibooks. Also, for all future reference, the content here is now being released under ghe GNU Free Documentation License.

Layman's terms
Needs some information to make it accessible to laypeople. If not intended to be read by laypeople, should state prerequisite texts.
 * I'm not sure there is a whole lot that can be done there. Ideally as other genetic counselors visit the site and use these outlines they may update the outlines and flesh them out a bit, making this more accessible for non-experts.  But keep in mind this is a handbook for genetic counselors - so it is designed with experts in mind.

title: Talk:Handbook of Genetic Counseling


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User:Jrleighton

This is me.

title: User:Jrleighton


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Wikijunior talk:Ancient Civilizations/Atlanteans

too many spelling mistakes

Does this even belong here? I'm not sure a story with no corroboration told over two millenia ago rises to the level of being included as a "fact." I'm sorry if this has been discussed elsewhere, but I wanted to check. Rjstreet 04:00, 26 November 2005 (UTC)

I'm as big a fan of the Atlantean Story as anyone, but i'm not sure that including it in a book is a good idea. We Still have NO CLUE as to where Atlantis might be, its lost, precisly why we can't find it. Good Effort, but this page should be removed.

I also think this should be removed from "Ancient Civilizations" or better moved to some section for "fictive ancient civilizations" which would be intresting as well.

 * I would have to add that I don't think this really belongs here. Most of this can and ought to be incorporated into the Minoan module instead, as the Minoans are considered a very likely source of the Atlantean ledgends.  They are geographically close to Greece (you don't hear about Atlanteans from the Aztec or Myan cultures), and there is geological evidence that volcanic activity may have "destroyed" Minoan cities in historical times, giving a good scientific explaination as to what may have in fact happened to them and a potential source of Altantis ledgends.  And certainly even simply weapons like a Bronze sword may have been significantly advanced compared to what most of Greece had for centuries before Plato, not to mention that they would have been in contact with Assyrians, Babylonians, and Egyptians as trade routes from these empires would have gone through the Minoans on their way to Greece.  Writing systems and scientific knowledge from those other civilizations, with perhaps unique insights of their own, would have made the Minoans quite advanced in their scientific knowledge as well compared to the Greeks before their demise. --Rob Horning 13:24, 20 January 2006 (UTC)

I found this page in a state of relative dissarray and re-wrote it in a style that: A. Was more suitable for children B. Clearly emphasised the legendary and possibly ficticious state of the civilisation. C. Was, to my knowledge, grammatically correct with all poor spellings corrected. Please point out or correct personally any spelling mistakes that remain in the article.

It is unclear as to whether this page is discussing the original Atlantis page or my revised one, but as far as I can tell, all arguments here apart from the Minoan one are no longer relevant when looking at what I did to the page. I hope that this situation is cleared up to a satisfactory standard and I am more than willing to insert a section into the page about how it is easy to theorise that the Minoans may be the basis of the legend, with links to that page, copying this new part of the article largley from Mr Horning's above comment if I may. However, I do not think the article should be deleted. Anyone researching the Atlanteans may not be able to find the information they require if it is in the Minoan section. Without the knowledge of the Minoan theory, a reader might assume there is no information about the Atlanteans on the site at all and could go looking for information elsewhere. I hope you take these notes into account when making your judgement. For your reference, I had no idea that the image in the page was copyrighted and I did not publish it onto the page personally. And legend is definately the correct spelling...-- BB. 7th February 2006.

Image copyright violations
The images are in direct copyright violation. However I have found the artist and contacted him asking for permission to use them on this page. But if permission is not granted they will have to be deleted.--Konstable 05:45, 30 January 2006 (UTC)

 * Note that the text here is more or less original contributions, and that will not be deleted. All that is going to go is the images, which IMHO is no major loss.  --Rob Horning 13:37, 7 February 2006 (UTC)

atlantis
what if Atlantis was right under our feet and didn't even know this because of different ocean floor patterns of time? What if the civilazation is under another civilization of our time: like Troy? some things that are not found are covered. —The preceding unsigned comment was added by 74.67.97.46 (talk • contribs).

 * I would like to point out that as a serious study of ancient cultures, Atlantis barely fits in here. Plato is about the only "authoritative" source about Atlantis, and even that is mainly something that would otherwise be considered something of a Wikipedia-type stub article at best.  The rest is fictional conjecture and psuedoscience that makes UFO researchers seem like a paragon of scientific accuracy.

 * I will admit that I have some prejudice about even having this article included next to ones about ancient Egypt and Rome, as this seems to be something akin to purely fictional civilizations such as Narnia and Minas Tirith. The only difference is that Atlantis seems to have been discussed anciently and in mideval times as well, so there may be a small bit of truth to the whole thing.  I would emphasize that in particular for this article, some very substantal and credible sources ought to be used to substantiate any statements made about this civilization.  I have some serious dobuts that is even possible beyond Plato and his comments, but I may be surprised.  You certainly will be completely unable to find credible archeologists who have done any excavations of any Atlantean artifacts that confirm anything related directly to what Plato described, unless it is another civilization that already is known with another name and should be included with this Wikijunior book under that more commonly used scientific or popular culture name.  Please convince me (and others) that this article really needs to remain.

 * I'm not pushing hard for an immediate VfD here, but it may end up going that way. I'm willing to entertain that something of quality can be made from this article but in its current form this article is seriously wanting and in need of significant improvement and citations of scholarly sources.  --Rob Horning 19:15, 9 December 2006 (UTC)


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Help talk:Redirect to special page demo

Meta:Help:Redirect to special page demo authors and history
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 * User:Patrick

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text: User talk:67.129.254.1

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User:Agave Akula

Hi and welcome to my Wikibooks page!

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Paleontology

Paleontology is the study of prehistoric life. The primary way paleontologists collect new information is through the fossils of organisms.

Table of Contents
/What is Paleontology/

/Geologic Time/

/Fossilisation/

/Plant Fossils/

/Invertebrate Fossils/

/Vertebrate Fossils/

/Paleoecology/

/Taphonomy/

/Field Techniques/

/Careers in Paleontology/

/Glossary/

/References and Further Reading/

Paleontologia

title: Paleontology


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AT&T Mobility FAQ/MEdia Net Configuration

This is a setup guide for AT&T Mobility MEdia Net (as distinct from Data Connect). Important Notes:
 * This information is provided as a public service without warranty of any kind. Use at your own risk.
 * "Tethering" is discouraged, and AT&T reserves the right to deny service based on usage, including tethering. (See MEdia Legal Notices)
 * Items not covered here should be left at default values unless you really know what you are doing.

Differences between MEdia Net and Data Connect

 * MEdia Net uses the AT&T WAP profile (settings) to support most types of Internet access (e.g., HTTP [Web browsing], SMTP/POP3/IMAP Email, FTP, Telnet, SSH, SSL). However, not all protocols seem to be fully supported, so problems may be seen with such things as VPN], and Data Acceleration is not available. Note that MEdia will not work with AT&T Data Connect profiles. MEdia is less expensive than Data Connect (as of this writing).
 * Data Connect uses AT&T Data Connect profiles (settings) to provide standard Internet connections with AT&T as the ISP (Internet Service Provider). Connections can be configured with or without Data Acceleration (which significantly boosts throughput by means of image compression [which reduces image quality], caching, and transport optimization). Data Connect is more expensive than MEdia (as of this writing).

Handset (Phone) Configuration
If WAP isn't already working on the handset, the handset and SIM must first be configured for AT&T WAP:

 * This is best accomplished by asking AT&T Support (dial 611) to "push" WAP settings to the handset (normally done automatically by SMS when a WAP package [e.g., MEdia] is added to the account).
 * Alternative: Cingular On-line Phone & Device Support Select your Network, and handset Manufacturer and Model (or a similar device) to access Device Setup.
 * [appears to be discontinued] Another alternative (untested), for Sony Ericsson devices, is to use the Configurator on the Sony Ericsson website. Select Configurators, Phone model, WAP Read more, and then follow the prompts. (Email and MMS can also be configured this way.)

This configuration is sufficient for WAP and/or Web browsing with the handset alone. It's also sufficient for Email given an Email client in the handset that has been properly configured (including selection of the WAP profile for connections).

Using Windows XP Dial-Up Networking
''This is for an EGPRS(EDGE) handset. For HSDPA, see HSDPA Handset (Motorola V3xx) Configuration.''
 * Create a handset modem entry. If your handset connection (serial cable, USB cable, IrDA, Bluetooth) created a modem entry for your handset (e.g., Standard Modem over Bluetooth link), then you can skip to next major step (Create DUN connection); otherwise:
 * Obtain the latest handset modem driver.
 * Make sure your handset connection (serial cable, USB cable, IrDA, Bluetooth) is installed properly, and note the COM port assigned. Make sure the handset is connected and powered on.
 * Use Control Panel → Modem to Add the handset modem. Windows should detect the modem, and then search for the best driver. When it does, give Windows the location of the modem driver, and complete the installation. (If auto-detection fails, try to Add the modem manually using the appropriate COM port with the driver.)
 * Create a new Windows Dial-Up Networking (DUN) Connection:
 * Control Panel → Network Connections → Create a new connection

 * Network Connection Type : Connect to the Internet

 * Getting Ready : Set up my connection manually

 * Internet Connection : Connect using a dial-up modem

 * Selete a Device : (Select just your serial, USB, IrDA, or Bluetooth connection)

 * Connection Name : AT&T MEdia GPRS (or whatever you want)

 * Phone Number to Dial : *99# (uses default GPRS profile)

 * User name : WAP@CINGULARGPRS.COM (must be all uppercase)
 * Password : CINGULAR1 (must be all uppercase)
 * Confirm password : CINGULAR1 (must be all uppercase)
 * Make this the default Internet connection : (probably not)

 * Completing : Click Finish

 * Set the port speed. (Especially important for EGPRS/EDGE!)
 * See How To Set the Port Speed in Windows XP?

Use this Dial-Up Connection to connect your computer to the Internet with AT&T GPRS/EGPRS(EDGE).

Using AT&T Communication Manager (Handset)
''This is for an EGPRS(EDGE) handset. For HSDPA, see HSDPA Handset (Motorola V3xx) Configuration.''

AT&T Communication Manager is a software package that makes it easier to connect your computer to the Internet over AT&T. Available for free download (inc. help files on same download page). Includes drivers for mobile devices sold by AT&T.

Do not connect your mobile device before starting this procedure:
 * Install and launch the software : Select Configure a phone as a tethered modem.
 * Select the method of connection : This example is Bluetooth.
 * Connect your mobile device when instructed to do so : Give Windows time to recognize it before proceeding.
 * Device recognized and configured : With your mobile device showing in the box, click Finish.
 * Edit Connection Profile : You're not really ready to go yet because the port speed needs to be configured! Select Connections Edit → Connection Profiles
 * Profiles → Add : Profiles for Data Connect are pre-configured, but you'll have to add a profile for MEdia, so click Add.
 * GSM : Select AT&T Internet
 * Create Custom Profile
 * IP Settings : Leave both on automatic
 * General : Change the Profile name to whatever you want (e.g., AT&T MEdia), set any other options as desired, and click Finish.
 * Launch your new Profile : Select (verify settings) and click Connect.
 * Connected! : You should now be connected to AT&T MEdia.

Using BVRP/Motorola mobile PhoneTools
''This is for an EGPRS(EDGE) handset. For HSDPA, see HSDPA Handset (Motorola V3xx) Configuration.''

 * BVRP mobile PhoneTools works with a wide range of devices.
 * Motorola mobile PhoneTools (branded version of BVRP mobile PhoneTools) works only with Motorola devices. (Low-cost sources include Shopoem.)

Illustrated with Motorola V551:
 * Create Internet Connection : After starting mobile PhoneTools, click the Internet Connection icon.
 * Launch it : A new Internet connection should be created automatically. Launch it to test it.
 * Connection opening: Here's how it should look while launching the new Internet connection.
 * Completed
 * This process should create a standard Windows Dial-Up Networking (DUN) connection that can be managed and used in Windows (Control Panel → Network Connections) without having to launch mobile PhoneTools. Be sure to set the port speed...

 * Set the port speed. (Especially important for EGPRS/EDGE!)
 * See How To Set the Port Speed in Windows XP?

HSDPA Handset Configuration
''This is for an HSDPA handset. For EGPRS(EDGE), see Handset (Phone) Configuration.''

Configuration of a HSDPA handset (e.g., AT&T-branded Motorola RAZR V3xx) for Windows Dial-Up Networking is different from the EGPRS(EDGE) handset configuration above (which would result in Error 734).
 * 1) Prepare to install handset "modem":
 * 2) Bluetooth: Windows XP SP2 Bluetooth stack is recommended, not a third-party Bluetooth stack (e.g., Widcomm).
 * 3) USB: Be sure to install proper USB modem driver (e.g., Motorola USB Modem) before connecting handset.
 * 4) For Motorola handsets, install Motorola USB modem driver from Motorola USB Drivers
 * 5) If Motorola Phone Tools or Cingular Communication Manager is installed after the MOTODEV driver, reinstall the latest MOTODEV driver.
 * 6) Install handset "modem"
 * 7) Bluetooth:  Pair handset with computer using Windows XP SP2 Bluetooth stack, which should install "Standard Modem over Bluetooth link".
 * 8) USB:  Connect handset to computer with USB cable, which should automatically cause Windows XP SP2 to install handset USB modem. (Motorola RAZR V3xx uses standard 5-pin mini-USB cable, and Motorola USB Modem is installed.)
 * 9) Configure handset "modem":
 * 10) Right-click My Computer.
 * 11) Click Manage.
 * 12) Click Device Manager.
 * 13) Expand Modems section by clicking its [+].
 * 14) Double-click handset "modem".
 * 15) Click Advanced tab.
 * 16) Put in Extra initialization commands: AT+CGDCONT=1, "IP", "WAP.CINGULAR"
 * 17) Click OK.
 * 18) Close Computer Management.
 * 19) Create "dial-up" connection:
 * 20) Open Control Panel.
 * 21) Double-click Network Connections.
 * 22) Under Network Tasks, click Create a new connection.
 * 23) When New Connection Wizard starts, click Next.
 * 24) Select Connect to the Internet (if not already selected), and click Next.
 * 25) Select Set up my connection manually, and click Next.
 * 26) Select Connect using a dial-up modem, and click Next.
 * 27) Check the handset modem; uncheck any other modems; and click Next.
 * 28) Enter name for this connection (e.g., "AT&T MEdia"), and click Next.
 * 29) In Phone number enter *99# and click Next.
 * 30) Leave User name and Password blank; set options as you wish; and click Next.
 * 31) Click Finish to launch the Connect dialog box.
 * 32) Configure "dial-up" connection:
 * 33) Leave User name and Password blank; check Save this user name; select option you prefer; and click Properties.
 * 34) Click Configure button next to All devices call the same numbers
 * 35) Select maximum speed (e.g., 921600); and click OK. The latest version of the Motorola USB modem driver now permits full USB speed to be selected.
 * 36) Uncheck Enable hardware flow control. (No options on this tab should be checked.)
 * 37) Set any other option(s) you wish, and click OK.
 * 38) Click Dial to test the connection.
 * 39) Close Network Connections.

Using AT&T Communication Manager (PC Card)
Use the procedure in Using AT&T Communication Manager (Handset), selecting PC Card as the method of connection

Using Sony Ericsson Wireless Manager
Works only with Sony Ericsson PC Card devices:
 * 1) Install the Sony Ericsson Wireless Manager:
 * 2) * This is best accomplished by downloading the latest version from the Global support area of the Sony Ericsson website. Select Location, Enter product name and click on the appropriate Matching products link, Software, Applications, Wireless Manager, Download here, and Download.
 * 3) * Or use the CD that comes with the PC Card.
 * 4) When the Wireless Manager is run for the first time, the Connection Wizard will start automatically. Enter the following settings:
 * Create a new connection : AT&T MEdia (or whatever name you prefer)

 * Type of Connection : GPRS (selects the default GPRS profile)
 * Choose network : Other

 * Primary APN : wap.cingular (must be all lowercase)

 * User ID : WAP@CINGULARGPRS.COM (must be all uppercase)
 * Password : CINGULAR1 (must be all uppercase)
 * Save password : Check

 * Finish

Use the Wireless Manager to connect your computer to the Internet.

Email

 * The usual problem when sending email from a handset with SMTP capability is the outgoing SMTP server. Thanks to spammers, outgoing SMTP servers now generally require some form of authentication when you're off the provider's network. You should be able to find out what kind(s) of authentication are supported by contacting the email provider (e.g., your ISP). Finding out what your handset supports may be a bigger challenge—documentation is often woefully inadequate in this area.
 * If the email provider supports POP3 before SMTP authentication, then you need to find a way to have the handset do a POP3 check or download before sending mail.
 * Some handsets (e.g., Sony Ericsson Z600) now have support for SMTP-AUTH (Authenticated SMTP, different from POP3 before SMTP). For this to work, you usually need to configure the handset with a valid mailbox id and password for the email provider.
 * On the AT&T network you can use cwmx.com (preferred, no footer added) or photo.mycingular.com (adds a photo messaging footer) as an outgoing SMTP server. Since you're authenticated by being on the AT&T network, no further authentication is required.

Speed

 * Handsets and PC Cards do not all have the same data performance—maximum speeds are limited by GPRS/EGPRS/EDGE Multislot Class](and the carrier). In general, all reasonably recent GPRS/EGPRS/EDGE-capable devices from Ericsson and Sony Ericsson support Class 8 (4+1) and Class 10 (4+2, max of 5), whereas most Nokia devices (as of this writing) are limited to slower Class 4 (3+1) and Class 6 (3+2, max 4). Motorola has both Class 4 and Class 8 devices. (The first number is the maximum number of downlink slots, and the number after the "+" is the maximum number of uplink slots.) This can translate into a substantial difference in throughput—if supported by the carrier, Class 8 is 33% faster on downlink than Class 4.
 * Connections between handsets and "tethered" devices (e.g., notebook computer, PDA) are typically implemented as a serial port, either real or virtual, and port speed usually defaults to 115 Kbps. (Bluetooth is typically implemented on a computer as a virtual serial port that will go as fast as 921.6 Kbps, but which runs at only 115.2 Kbps by default.) While 115 Kbps is generally fast enough for GPRS, it can be a bottleneck for EGPRS(EDGE) (as well as UMTS/HSDPA). In general, port speed should be at least 230 Kbps for GPRS and 460 Kbps for EGPRS(EDGE) (920 Kbps for UMTS/HSDPA).

WAP

 * WAP as built into many handsets is much more limited than standard HTTP—much of the Internet (World Wide Web) cannot be accessed through WAP.


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User talk:204.229.240.120

Please stop. If you continue to vandalize pages, you will be blocked from editing Wikibooks.

title: User talk:204.229.240.120


text:
Bookbinding/Long stitch

This module covers the making of a long-stitched soft-board binding. This style was recommended for small-scale projects by the book conservation lab at the University of Iowa.

If there are professional bookbinders in your area (and most large cities have them), you should be able to get your book bound for somewhere on the order of $20. Professionals have machines and supplies to do a case binding on fairly short order.

Cover
The cover for a long-stitched binding is made of cardboard -- specifically acid free two ply museum board. In determining the size of the cover, you have to allow for not only the thickness of the paper, but the thickness of the thread used to sew the binding, so now is the time to get the thread. The thread should be heavy, heavy enough that you might be as likely to call it fine cordage as you are to call it heavy thread! Thread diameters of close to a millimeter (when uncompressed and not under tension) are quite reasonable. The thread should compress to about 1/2 millimeter when successive turns are wrapped tightly around a pencil. See the section on thread for other criteria.

If you have 19 sections, as in DEC's 1973 Introduction to Programming, you'll need to add the thickness of 19 threads to the thickness of your book. To find this, wrap 19 turns of thread tightly around a pencil and measure the length of the wrapping, then add this to the thickness of the clamped spine of the stack of sections that will make up your book.

The museum board has the interesting property that it flexes fairly easily in one direction but it is fairly stiff in the other. You want your cover to flex easily from side to side, since that's the way you tend to bend the covers of a book when you hold it open to read. You want the book to be stiff from top to bottom, since bending in that direction should never happen. Taking this into account, cut a rectangle of museum board with the dimensions shown in Figure 4.1:

Do not cut the cover oversize. The cover used with this style of binding is intended to cover the pages of the book in the way a conventional paperback cover does, with the edges of the cardboard exactly even with the edges of the bound pages.

I did all my cutting with a carpenter's square to guide a large X-acto knife. It took two or three scores with the knife to cut all the way through, and I used an old cardboard sheet as backing so I wouldn't cut into the top of the table I was working on. A paper cutting guillotine also works well to cut out the cover, particularly the type of guillotine that clamps the material being cut so that the blade does not pull the cardboard sideways as it cuts.

Having cut out a rectangular piece of cardboard, you need to score the creases where the cover will hinge to wrap around the pages. I measured twice to avoid error, then set my straight-edge along the planned hinge lines and used a blunt tool to score the crease. Traditional bookbinders would use a bone tool for this. I used the rounded and polished end of a metal ruler I found in my toolbox. Be careful not to cut or tear the fibers of the board when you score it; your goal is to compress the fibers in order to guide the crease. Figure 4.2 shows the cover with scored creases.

Before you bend the cover, you need to cut a series of equally spaced square-ended slits in the cover, as shown in Figure 4.2. Typically, these should be about an inch apart, (anywhere from 2 to 3 cm will do) and the slits at the top and bottom should be a bit closer to the top and bottom edges of the book (about 1/2 inch or 1.5 cm is nice). Each slit should be about 1 mm wide, but the precise width is less important than the uniformity.

I cut 8 slits for this purpose, but 7 would be just as good. The ends of the slits should be about 1/2 the thickness of one section of your book from the creases that you just scored in the cover.

There are several ways to cut these slits. For my first effort, I used an X-acto knife, but I've found that cutting cardboard with a hammer and chisel is very fast and accurate. Use a broad-bladed wood chisel that's almost the length of the slit you want, and make sure it's very sharp. Place the chisel so the flat side faces the side of the slot you are keeping, and the beveled face faces the waste material you will discard. Always work against a disposable backing that won't damage the chisel; I use some heavy strathmore board for this. Practice a bit on scraps of your cover material before you attack the real thing.

Another way to make these slots was suggested to me by Neil Tyler. He has done this with an inexpensive utility knife, the kind with a cast metal handle that is in two halves held together by a screw. Normally, you put only one blade in such a knife, but if you put two blades in, side by side, with a spacer between them, you can cut slots that are about as wide as the thickness of the spacer plus the thickness of one blade. There is one warning about this method! Be extremely careful! Wounds made by closely spaced parallel blades are nasty, difficult to bandage and slow to heal when compared with the commonplace cuts that most users of sharp tools have experienced on occasion.

Punching holes
Edit this section. Paper is hard stuff, and pushing a sewing needle through 8 layers is no fun; it is far easier to pre-punch each section for sewing! To do this, make a jig out of a scrap of cardboard with a very straight edge.

 * 1) Cut a shallow wide notch in the cardboard. The depth of the notch should be about the thickness of the 8 sheets of paper that make up your sections.  The width of the notch should be the height of the spine of the book.
 * 2) Lay out the holes that will be punched, making a mark for each one on the edge of the cardboard. In the case of a long stitch binding, these measurements can be transferred directly from the cover as follows:
 * 3) *Put the jig parallel to the length of the part of the cover that will be the spine, so the notch just brackets the cover.
 * 4) *Carefully mark where each slot in the spine passes your jig.
 * 5) Make a V shaped notch at each mark. These notches show where the holes go in the crease of each section.
 * 6) It's a rare day that you can get the jig (or the slots in your spine) perfectly symmetrical, so mark one end of your jig as the top, so that you can punch all of your sections the same way. Always make the up direction point towards the top of the page, and your book will come out with even edges.

Figure 5.1 illustrates the finished punching jig, resting against the spine of the cover:

The purpose of the V shaped notches is to guide the tip of an awl as you punch holes in your sections. Slide your jig into the center of a folded section until the notched edge rests in the crease, then hold the back of the section against a scrap of wood and use a good sharp awl to punch a row of holes, one per notch in the jig. Keep the section folded fairly tightly, and the awl will find the center of the crease in the section and the center of the notch fairly naturally.

Sewing
The long stitch I used is a fairly modern modification of an ancient style of bookbinding; the basic rules are simple: Sections of the book are sewn into the cover one at a time, in sequence, from the front of the book to the back, using a single length of thread to sew the entire book. In sewing each section, the thread runs once down the length of that section, alternately inside the fold of the section and outside the spine of the cover.

The thread is always sewn inside the fold of the section at each end of the book; except at the ends, the threads of successive sections alternate, so that the sewing pattern on the back of a finished book (with 4 sections in this example) should look something like is shown in Figure 6.1:

The book is sewn with a single thread, between the indicated points. Note that it takes a bit of cleverness to sew the ends of the sections, since the natural alternation of over and under brings the thread out somewhat randomly in one or the other orientation.

The thread should always pass over the end of each section and around the end of the spine. This helps prevent the pages from tearing out, because tears almost always begin at the end of the crease.

Before you start sewing, you need to measure out enough thread to sew the entire book. For a book with 19 or 20 sections, wrap the thread 10 times around the handfull of sections when they're clenched tightly in the cover. Then wrap one or two turns for good luck. It's better to have a bit of extra thread than to have to knot the thread in midbook!

Before you start sewing, it helps (but is not strictly necessary) to wax the thread with beeswax.

A note of caution: You do your final quality control check when you commit yourself to sewing in a section! Once the wrong section is sewn in or the right one is sewn in with a missing or inverted page, it's no fun to undo. Check what section you are sewing, and make sure it is all there and right-side up! As you gain experience, you'll find that you spend less time checking, but it's better to do too much checking than too little.

Also, with each section, check that all the pre-punched holes line up with the slits in the cover. If they don't you've probably got the section upside down. If they still don't line up, you've done a bad job punching the holes, and you'll have to repunch a few.

Figure 6.2 shows, in some detail, is a cross section of the knotting at the end of a thread:

Try to keep the knot and the loose end on the inside of the book. A tight square knot will do well here. Start by making the knot at one end of the first section, and finish sewing the first section to the spine. At the end, you'll face a problem -- how to finish one section and start the next.

Here, in some detail, is the sewing pattern used to change from one section to the next. If the thread emerges from the end of a section in the crease of that section, go outside the cover and down into the first prepunched hole in the next section, then out the crease, over the spine, and through the same hole as you begin sewing the length of the next section.

If the thread emerges from the end of a section outside the spine, go around the end and down the crease, re-using the last hole in the same section before going outside, around the end of the next section, and up the crease.

In both cases, the above sewing pattern will produce the result shown in Figure 6.3.

Here, dashed lines are used to show threads that are tucked into the crease of a section, while double horizontal and diagonal lines show the threads visible from the outside of the spine.

Whenever you use the same hole twice, always be sure not to sew the thread through itself. Pull the thread that goes through the hole off to one side, then thread the needle through to the other side of the same hole. If you do accidentally sew through the thread, it will make it difficult to tighten the thread when you're done sewing.

As you reach the end of the book, it will get hard to squeeze the last few sections in. You'll have to press hard to move the already bound pages down the spine to make room for the last sections, and as you work on the very last one, you'll have to squeeze the book again each time you try to get the needle through. If you measured the spine width correctly, you'll just barely manage to fit the last section in -- that's the test of a perfect fit.

If you run out of thread before you reach the end of the book, follow the instructions below for tightening the thread before you tie on a new length of thread, then tie the knot (a square knot) as close as you can to the last hole the thread passes through, Keep the knot on the inside of a crease! Do not back yourself into the situation where you have a knot that you need to pull through a hole in the sewing when you try to tighten the thread later.

Before you tie the final knot in the book, tighten the thread, working along the spine from the initial knot towards the end, pulling out any slack until the thread is uniformly tight throughout the sewing. I use a sharp awl (the same one I used to punch the holes in the sections) to do this, since it is easy to insert the tip under a tight loop of thread and pull the slack forward to that loop, tightening the previous loop. You don't need to pull too hard, but you don't want to leave any slack in the binding.

Finally, when the sewing is uniformly tight, tie the final knot, and you have a book! If the pages aren't in the right order at this point, though you'll have trouble fixing the order without cutting the thread and re-sewing!

The spine of the finished book is shown in Figure 6.4. Note that the end sewing and the threads holding the center sections of the book match almost perfectly with the pattern illustrated in Figure 6.1. The pattern of the threads holding the very first and last sections is somewhat obscured by the tighter packing of these lines of sewing.

The book shown in Figure 6.4 has seen several years of use, and the impact of this wear is quite visible. Repeated flexing of the fold where the book front meets the spine has torn some of the surface fibers. Should this crease ever begin to tear, it would be a simple matter to thread linen tape through the sewing and glue it to the front and back covers in order to reinforce the spine and hinges. The photo shows no wear on the threads, and the torn fibers along the crease are very clean; this is because the book has been protected by a dust jacket since it was bound.

title: Bookbinding/Long stitch


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Digital Circuits/Common Integrated Circuits

This page will talk about some common integrated circuits, including where to buy components, form-factors, etc...

DIP, PDIP, SPDIP

DIP stands for "Dual Inline Package", and is what common Integrated Circuits come as. The "P" Prefix means the chip will be plastic, the "S" prefix means it will be thinner then a normal DIP, or it will have pins that are closer together. Occasionally packages will be found called "CERDIP", where the "CER" prefix means that the package is made of ceramic, and is therefore more resistant to heat. CERDIPs are more expensive then PDIPs, but are less susceptible to heat and static charge.

SSOP
SSOP stands for Small Shrink Outline Package.

SOIC
SOIC stands for Small Outline Integrated Circuit.

Distributors
Mouser Electronics, Digikey, Futurlec, Jameco, SparkFun

Manufacturers
Out of many, many, different manufacturers around the world, some of the most common are:

 * Texas Instruments (home to the first integrated circuit)
 * Fairchild Semiconductor
 * Maxim Semiconductor
 * Xilinx
 * ON Semi
 * Mitsubishi
 * Analog Devices
 * STMicroelectronics


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Bookbinding/Museum board

Museum board is a special type of cardboard. Specifically, it is a white, acid free cardboard with the interesting property that it flexes fairly easily in one direction but it is fairly stiff in the other. This is because of the grain of the paper fibers. Denny Jones recommends two ply museum board for long stitch binding. Good art-supply stores carry this. One sheet will make about eight book covers for books printed on standard sized typing paper.

title: Bookbinding/Museum board


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Cookbook talk:Carrot Paprika Spread

[quote]You might want to add lecithin powder as an emulsifier[/quote] lecithin is made from EGGS. it ain't vegan...

 * The ingredients list it as "soy lecithin" so I don't think that's a problem. Jessicapierce 11:12, 30 April 2007 (UTC)

"Parpika" / "paprika"
As I understand it, these words refer to the same thing. But this recipe calls for "one parpika(s)," which the cook is to mash. This baffles me as I only know paprika as a powdered spice. Can anyone explain this ingredient? Jessicapierce 11:12, 30 April 2007 (UTC)
 * Paprika really just means a pepper of the capsicum family. The powdered stuff is any of those fruit, dried and crushed; you can get hot, sweet, or mild paprika. "One paprika" would be like one bell pepper, or perhaps one sweet pepper (Italian pepper). Webaware talk 15:14, 30 April 2007 (UTC)
 * Thanks! I knew the source of the dried spice, but had never heard "paprika" used to refer to the fresh veg itself. Now I know! Jessicapierce 14:36, 2 May 2007 (UTC)

Might want to add some serving suggestions.

title: Cookbook talk:Carrot Paprika Spread


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Utopia/Tech Roadmap

Road map to a technological utopia
In man's eternal journey to a fuller understanding and control of the world around him certain new technologies have been developed and will be developed that vastly change almost every aspect of human life. To start we should cover those vital gifts of science which mankind already benefits from, the first foundation stone of all society is surely communication.

Communication
Early man soon set himself apart from the other animals and rose to the top of the food chain with the effective use of team-work. A team of maybe six pre-historic hunters armed with spears could confuse and overwhelm even the largest of prey by using only the most basic of communication and planning skills. In modern times communication has become an art form, indeed a plethora of art forms; oration, poetry, prose both fiction and factual even separating over time into such specialties as political, technical, short hand and a myriad of archaic almost forgotten variants. Communication could be said to be the first and still most important invention of humanity.

In the technologically advanced twentieth century communication developed a new front; the fast developing field of communicating with computers, new languages especially for this task were created. How ever it was not only computers that inspired new languages, short hand was developed to allow secretaries to take memos at great speed. Created using a simple system of easy to draw symbols for commonly used words it was a mild revolution in the office and foreshadowed the invention of the Dictaphone as a time saving tool for executives on the move. Like short hand the language ‘Lojban’ was invented to stream line language for better use in a specific purpose, while short hand increases speed Lojban increases accuracy and logic. The phrase ‘cute little girls school’ for instance has 22 connotations in English while in Lojban you could only say one precise meaning e.g. the school for girls who are both little and cute or the school which is little and cute and for girls.

In any kind of utopia good communication would be a vital thing; many attempts have been made to enforce an attempted utopian regime by controlling communications, Nazi Germany developed propaganda into an art form and made the use of it on both the enemy and the home state standard practice. George Orwell even theorized in ‘1984’ that language could be used in a more sinister way to subjugate the masses, he suggested that if someone could not say something then they wouldn’t be able to think that thing and so by removing certain phrases from the language thus any rebellion would be literally – unthinkable.

title: Utopia/Tech Roadmap


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Handbook of Genetic Counseling/Choroid Plexus Cysts on Ultrasound

Choroid Plexus Cysts on Ultrasound

Introduction and Contracting

 * Ask how the pregnancy is going
 * Ask about dates
 * Explain the session
 * Getting family hx/pregnancy hx
 * Talking about what a chorioid plexus cyst is and what it means for the pregnancy, testing that may be offered
 * What questions do you have?

Pregnancy hx

 * Any illnesses?
 * Any infections/exposures?
 * Any medications?
 * Verify dates
 * Screening tests up to now…ultrasounds? Triple screen test?

Family hx (probably at end of session)

 * Get two generation pedigree
 * Determine any risks to pregnancy
 * Specify any particular ethnic concerns as well

Choriod Plexus Cysts (probably at beginning of session)

 * What have you heard about them?
 * The Choroid plexus
 * A spongy layer of cells and blood vessels along the edge of the ventricles (pockets or spaces in the brain
 * Produces the cerebrospinal fluid that fills the ventricles and provides a cushion to the brain and spinal cord.
 * Development starts at 6th week
 * By 9th weeks the choroids plexus fills ~75% of lateralventricles
 * Starts to slowly decrease in size and by 20th week the chorioid plexus has assumed its adult form
 * Choriod Plexus Cysts
 * Description
 * Caused by folding of the spongy layer = trapping fluid in the area
 * BENIGN!!! They do not cause any problems for the fetus
 * Usually <1cm in size
 * Can be unilateral or bilateral
 * Usually can be detected by 11th week of pregnancy
 * usually resolve by the 24-28th week of pregnancy
 * Incidence
 * Found in 1% of pregnancies scanned between the 16th - 20 week.
 * Found in 50% of autopsies (fetuses, adults, elderly)
 * Association with chromosomal abnormalities
 * HIGHLY controversial
 * Trisomy 18
 * ~45% of fetuses with Trisomy 18 had chorioid plexus cysts
 * does not depend on gestational age, unilateral or bilateral or size
 * 1-2% risk of a chromosomal abnormality when CPC are found. Most likely Trisomy 18 if anything
 * TRISOMY 18 the syndrome
 * Describe genes and chromosomes
 * 1/3000-1/7000 live births
 * most do not survive to term
 * if live birth, usually die in days,weeks following birth
 * 90% die within the first year of live
 * severe congenital anomalies
 * 90% heart defects
 * severe mental retardation
 * 70-77% babies with Trisomy 18 will have other findings on ultrasound (some studies say ~100% after 24 weeks)
 * clenched fists
 * heart defects
 * rocker-bottom feet
 * omphalocele
 * hydrocephalus
 * VERY CONTROVERSIAL- relation to Down syndrome (thought to be coincidental by most authors)
 * Very rarely seen to be related to CPC cysts
 * 1/660 live births
 * DS - the syndrome
 * Mild-moderate MR
 * Heart problems in 40%
 * Characteristic facial features
 * Ultrasound findings
 * Echogenic bowel
 * Femur length
 * Nuchal fold thickness

Discussion of triple screen results (if they are present)

 * SCREENING test - NOT diagnostic
 * Measuring three values of proteins in the mother'sblood
 * They are produced by the baby in its liver
 * MoM values of 1.0 are the standard
 * Maternal age and gestational age are considered
 * For risks associated with Trisomy 18 = expect all three values to be low
 * Your results show (no/an) increased risk over the general pop of mothers who are your gestational age.

Risk of having a baby with Trisomy 18

 * Consider maternal age
 * Consider CPC
 * Consider triple screen results
 * Consider presence of other markers on ultrasound
 * USE CHART (see attached or ask Kris for a copy of hers)

Testing Offered

 * Detailed ultrasound to look for other markers (previously discussed)
 * Amniocentesis
 * Risk 1/200
 * Determines presence or absence of aneuploidy
 * Does not guarantee a healthy baby
 * Some centers debate about offering based solely on CPC

Important Points

 * 18% of unaffected fetuses will have more than just CPC on ultrasound!!!!!


text:
Talk:Utopia

I've started revising parts of this book and overhauling the structure. KevinBaker 20:24, 19 August 2006 (UTC)

title: Talk:Utopia


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Handbook of Genetic Counseling/Classical Myotonic Dystrophy

Classical Myotonic Dystrophy

What is myotonic dystrophy?
Myotonic dystrophy (DM) is the most common adult form of muscular dystrophy. It is a multisystem disorder that affects the muscles, as well as the eyes, heart, endocrine system, and central nervous system. Myotonic dystrophy causes muscle weakness accompanied by myotonia, a delayed relaxation of muscles after contraction. Myotonic dystrophy, also known as Steinert's disease and dystrophia myotonica, is a hereditary condition. .

What causes myotonic dystrophy?
Myotonic dystrophy is caused by a defect in a gene called DMPK. The gene has a stretch of DNA that contains a series of CTG repeats in its sequence. Normally, the DMPK gene has less than 37 CTG repeats. However, individuals with myotonic dystrophy have more than 37 repeats, making the gene unstable. The greater the number of repeats that an individual has, the more severe the symptoms will be. Genetic anticipation is often observed in the inheritance of myotonic dystrophy. Anticipation means that the number of repeats tends to increase as the disease is passed from one generation to the next, leading to increasing severity of symptoms and decreasing age of onset. Anticipation is most commonly observed in the transmission of myotonic dystrophy from maternal genes.

How does a person get myotonic dystrophy?
Because myotonic dystrophy is a hereditary disorder, it is transmitted from generation to generation. The defective gene is dominant, meaning individuals who inherit the gene from either their mother or their father will have the disorder. If one parent has the disease, there is a 50% chance that myotonic dystrophy will be passed on to their offspring.

What are the symptoms of myotonic dystrophy?
The effects of myotonic dystrophy vary widely, even among members of the same family. Some individuals have symptoms so mild that they hardly notice them. In other individuals, muscle weakness and wasting may cause more severe disabilities. In general, the older a person is when muscle weakness becomes noticeable, the slower the disease progression and the less serious the effects. Myotonic dystrophy is loosely classified into three categories based on the number of CTG repeats in the gene, the severity of the symptoms, and the age of onset. The three forms are: mild, classical, and congenital.

What are the characteristics of classical myotonic dystrophy?
Individuals with classical myotonic dystrophy have 100-1500 CTG repeats in the DMPK gene. The age of onset is typically between 10 and 30 years. The predominant symptom is muscle weakness and wasting which usually begins in the distal limb muscles, including the forearms, hands, feet, and ankles. This muscle weakening may lead to foot drop and difficulty performing tasks requiring hand dexterity. Muscle weakening may also be observed in the neck or shoulders. Very rarely, the disease may progress to the point where an individual is confined to a wheel chair. Myotonia is also observed and may lead to difficulty performing some daily activities. Individuals with myotonic dystrophy often have long, thin faces, and weakness of the muscles in the eyelids may cause them to droop. Some men with myotonic dystrophy experience frontal balding. Other symptoms that individuals may experience include speech problems, cataracts, and cardiac arrhythmia. Myotonic dystrophy may also lead to constipation, diarrhea, or gallstones. In the later stages of the disease, some people experience sleep apnea and hypersomnia. Women with myotonic dystrophy have an increased risk for pregnancy complications. Problems may include an increased risk for spontaneous abortions, prolonged labor, a retained placenta, and post partum hemorrhaging. Men may experience testicular atrophy, although myotonic dystrophy has not been associated with an increase in infertility. Hyperinsulinism and abnormalities in the secretion of growth hormones have also been observed, but they rarely cause clinical problems. Learning problems have been associated with classical myotonic dystrophy. Also, obsessive compulsive, passive-aggressive, and avoidant behaviors have all been observed in some individuals with the condition. Individuals with myotonic dystrophy may have a shortened life span. The average age of death is 48-55 years old. Common causes of death include pneumonia, respiratory failure, cardiovascular problems, sudden death arrhythmia, and tumors.

How is myotonic dystrophy diagnosed?
A physical examination may reveal muscle weakness and myotonia. A special test called a muscle biopsy can confirm the diagnosis. Also, DNA testing can be performed to determine the number of CTG repeats on the DMPK gene. This blood test is 100% sensitive and specific. Presymptomatic testing is available for individuals who have no features of the condition but have a family history of myotonic dystrophy. Prenatal testing is also available.

How is myotonic dystrophy treated/managed?
Currently, there is no treatment for myotonic dystrophy. Muscle weakness can be managed with orthotics or other assistive devices. Treatment is available for many symptoms of myotonic dystrophy, including cataracts, diabetes, hypothyroidism, sleep apnea, and myotonia. In addition, close monitoring of the heart with an annual EKG, the eyes with an annual ophthalmologic exam, and screens for glucose concentration can provide early identification of some potential effects of myotonic dystrophy.

What informational and support resources are available?

 * Muscular Dystrophy Association
 * 3300 East Sunrise Drive
 * Tucson, AZ 85718-3208
 * (800) 572-1717
 * Email: mda@mdausa.org
 * [Web: http://www.mdausa.org/]

 * Myotonic Dystrophy Website
 * [www.umd.necker.fr/myotonic_dystrophy.html]

 * NCBI Genes and Disease Webpage
 * [www.ncbi.nim.nig.gov/disease/Myotonic.html]


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Handbook of Genetic Counseling/Cleft Lip and Palate

Cleft Lip and Palate

Review Medical History
(fill out remainder of intake and verify info)

Family History
(verify pedigree if we have one in his mother's chart or make a new one)
 * Be sure to include:
 * cleft lip and palate
 * heart defects
 * birth defects
 * learning difficulties
 * intellectual disability
 * miscarriages
 * early deaths
 * consanguinity

Inheritance and Recurrence Risk

 * If neither parent has a cleft than the inheritance is probably either multifactorial or recessive and these are not distinguishable usually
 * multifactorial -- combination of genes and environment
 * approximately 3-5% chance of having another similarly affected child this is 20-35 fold increase over baseline
 * (this risk increases more if the couple have more than one affected child)

Multifactorial Risks of Cleft Lip/Palate

 * recurrence also influenced by how severe the cleft is 5.6% for bilateral lip/palate, 4.1% for unilateral lip/palate and 2.6% for cleft lip without cleft palate
 * if it can be established that there are no other affected relatives, the risk to siblings (2.2%) is less than the overall risk (4%).
 * The higher figure should be used if the history is unreliable or unavailable.
 * If there is a third first degree relative than autosomal dominant or recessive inheritance should be considered.
 * recessive inheritance
 * both parents contribute the same recessive gene to affected child
 * recurrence risk 25% or 1:4
 * gene not mapped
 * Autosomal dominant -THIS IS WHAT WAS COUNSELED FOR THIS FAMILY
 * usually one parent will also have cleft
 * risk of recurrence is 50% or 1:2
 * gene mapped to short arm chromosome 6
 * X-linked recessive
 * pattern seen sometimes with clefting of the secondary palate or bifid uvula
 * x-linked recurrence risks
 * in one of these families from Iceland the single gene has been mapped to the long arm of chromosome X
 * Association with a syndrome or collection of physical findings which run together in the same person, and for the most part are seen in all individuals who have that syndrome
 * Syndromes are more common in cleft palate alone than in cleft lip with or without cleft palate, but can occur in any of these
 * Syndromic clefts are commonly inherited as single gene defects, but they can be due to changes in the baby's chromosomes, something used during pregnancy or a sporadic change

Prevalence of Clefts

 * 1:700 live births over 5,000 in US each year
 * between 1/5000 and 1/1000 for cleft lip and/or cleft palate, and about 1/2500 for cleft palate alone
 * more common among Asians 1: 500 and certain groups of American Indians 1:300 than among Caucasians 1:800
 * occur less frequently among African-Americans 1: 2000
 * Cleft lip and cleft palate together are more common in boys 3:2 ratio

Cleft Repair

 * cleft lip-- usually be repaired in the first few months of life-- for most infants with cleft lip alone, the abnormality can be repaired within the first several months of life (usually when the baby is 10 to 12 pounds)
 * cleft palate repairs are usually done between the ages of 9 and 18 months, but before the age of 2
 * exact timing of these repairs depends on the baby's health and considerations of his or her future development and will be decided by surgeon

Feeding Problems

 * Feeding difficulties occur more with cleft palate abnormalities
 * some babies with clefts have very few or no problems feeding
 * others have more difficulty --the infant may be unable to suck properly because the roof of the mouth is not formed completelely
 * breastfeeding is possible, but the use of special bottles and careful positioning of the baby are sometimes helpful modifications-- there are many types of bottles and nipples on the market that can assist with feeding an infant with cleft palate
 * Dr. Doktour recommended Haberman Feeder®
 * This is a specially designed bottle system with a valve to help control the air the baby drinks and to prevent milk from going back into the bottle

Hearing

 * important for ears and hearing to be examined on a regular basis because children with cleft palate are more susceptible to ear infections (otitis media) than children without clefts
 * Ear infections are often due to a dysfunction of the tube that connects the middle ear and the throat
 * Children with many ear infections are at risk for hearing loss, language delays, and speech problems because they are not able to hear language normally when fluid collects in the middle ear.

Teeth Considerations

 * only cleft lip-- teeth will probably not be affected
 * if affects the gums where the teeth grow - teeth may not erupt normally and probably need dental/ orthodontic treatments

Speech Difficulties

 * only lip --speech problems are unlikely
 * cleft palate over half need speech therapy at some point in childhood
 * many children who are born with a cleft palate develop normal speech by the age of 5
 * delay in both the onset of speech and the development of speech sounds during the first 9-24 months of age is not unusual
 * important to remember that some children, with or without a cleft palate, may simply develop speech more slowly than others.
 * important to talk to your child and to encourage your child to talk to you
 * before palate repair
 * there is no separation between the nasal cavity and the mouth and it can be difficult to learn how to make some sounds because the child cannot build up air pressure in the mouth because air escapes out of the nose and/or there is less tissue on the roof of the mouth for the tongue to touch
 * After palate repair
 * your child may be able to learn more consonant sounds and say more words
 * speech may still be delayed during the early years
 * articulation problems (difficulties in making certain sounds) may persist in some children throughout early childhood for a variety of reasons.
 * if teeth do not "line up" correctly, speech may be understandable, but some sounds (like "s" or "sh") may sound distorted or "mushy."
 * VPI (velopharyngeal insufficiency or inadequacy)
 * when speech is produced correctly, the soft palate lifts and moves toward the back of the throat, separating the nasal cavity from the mouth so that air and sound can be directed out of the mouth.
 * inability to close off the nasal cavity from the mouth is called velopharyngeal inadequacy.
 * characterized by hyponasal speech "talking through their noses."
 * occurs because when the soft palate cannot close off the nose from the mouth, air and sound can escape through the nose during speech
 * Approximately 25% of children with repaired cleft palates still show signs of velopharyngeal inadequacy.
 * grunt or growl sounds may be behavior that some children learn in an attempt to compensate for velopharyngeal inadequacy-- although it can be corrected by speech therapy it should be discouraged
 * Children with velopharyngeal inadequacy may also have a voice disorder.
 * voice may sound hoarse or "breathy" and may fatigue easily and is usually caused by the strain that he or she puts on the vocal cords while trying to build the pressure necessary for normal speech.
 * Speech therapy alone may be able to correct your child's speech disorder. Therapy can be extremely effective for children with mild hypernasality, an articulation disorder, or speech delay.
 * Speech therapy alone will generally NOT correct hypernasality that is caused by moderate to severe velopharyngeal inadequacy.
 * may require another palate surgery to help with speech
 * surgery is the most frequently-chosen approach for improving velopharyngeal function, but a prosthetic device may be an option for some patients.

Learning Difficulties

 * none expected it isolated cleft lip and palate
 * if part of a cluster of a syndrome learning ability is sometimes affected

Psychosocial Assessment

 * Having a baby can be pretty stressful especially when there are complications. How are you handling it?
 * Do you have help from your family?
 * Have you explained any of this to your friends or family?
 * Is the father of the baby involved in any way?
 * How is that?
 * Are you attending school?
 * Working?
 * The surgeries and treatment can get pretty expensive do you have health insurance coverage?
 * Other financial assistance?

Financial Assistance

 * Health insurance will pay for all or part of the necessary care
 * may qualify for BCMH
 * would probably qualify for WIC

Psychosocial Concerns

 * Initial shock and adjustment for the family
 * Often a period of mourning the anticipated child and the situation
 * Possibility of mother interacting differently and interacting less with infants with anomalies
 * Guilt - nothing you could have done to prevent or cause this
 * Feelings of concern, anxiety, and grief are not unusual
 * mothers of babies with clefts report more stress and more concerns about their competence as parents than mothers of healthy babies
 * reproductive plans generally unaltered by birth of child with cleft
 * later challenges as the child grows

Patient Resources
see attached

Differential Diagnosis
for up to 3% or both cleft palate
 * Van der Woude Syndrome
 * among most common syndromic causes of CL/P may be responsible
 * AD disorder gene mapped to long arm chromosome 1
 * presence of pits of the lower lip and cleft lip, cleft palate,
 * may also have neonatal teeth and missing teeth
 * development usually normal speech difficulties related to

Cleft Related Genetic Syndromes/Diseases
The following table was extracted from a table on Embryogenesis by Dr. Harold C. Slavkin; Director, National Institute of Dental & Craniofacial Research (NIDCR)


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Wikijunior:Ancient Civilizations/Scythians

What country did they live in?

The Scythians were a group of ancient tribes of warriors who originally lived in the steppes to the north of the Black Sea, in what is now southern Siberia. They were cattle-breeding nomads, meaning that they did not stay in the same place for long. When cattle ate out all the grass around, they travelled to a different place, where the grass was fresh and untouched. They were also skilled horsemen and brave warriors. They were the first who used light cavalry as a main military force.

The horse was everything for a Scythe. They started riding horses when they were small children. Horses were not just transportation for Scythians; they were their protectors, providers and best friends. When a Scythian warrior died, his horse was buried with him.

Scythian women were brave warriors as well. Living in the steppes was dangerous as you have literally nowhere to hide. Scythian women had to be strong and know how to protect themselves.

What did their buildings look like?

Scythians did not have buildings. It does not make sense to build a house if you know that you are leaving soon. They lived in tents instead.

The only buildings they left behind them were kurgans – artificial hills, made of stones and earth, elevated on top of the tombs of nobilities. These tombs were filled with everything that a person could need in the afterlife: clothes, dishes, weapons, golden jewellery. They cremated their dead by covering the body in wax.

What did they eat?
The favourite drink of Scythes was horse milk, often mixed with blood. They ate grains, fresh fruit, horse meat, and fish.

What did they wear?

Both men and women wore clothes that were comfortable for riding horse: leather pants and jackets, short soft boots tied at the ankle, and felt pointed hoods. Both men and women wore their hair long and loose, and men had beards.

Scythians also liked to decorate their clothes, horses and weapons with golden jewellery. Since Scythes were very close to nature, the main motif of their jewellery was animals. They loved to show animals in motion, because these images showed what Scythes valued most: strength, speed and freedom.

What did their writing look like?
Scythians did not develop any written form of their language. Though later, when they came in contact with other cultures, like the Greek colonies in the sea costs, they carved some texts in stones, but these were mostly for religious reasons and for the tombs. We don't know what their language was like and cannot read their writings. Their writing used the Greek alphabet with some modifications.

What did they believe?
Because the Scythians lived in constant danger, comradeship between warriors was important. Unrelated warriors swore an oath of blood brotherhood, after which they were committed to defending each other.

Herodotus recorded the seven Scythian gods and their Greek equivalent: -The chief god is Tabiti, the goddess of the hearth (like Hestia)

-Papaeus, almighty ruler of the heavens (like Zeus)

-Api is Goddess of the earth (Gaea)

-Goetosyrus (Apollo)

-Argimpasa (Aphrodite)

-Heracles

-Ares

Many Scythian mummies have been discovered in the Altai Mountains. When the Scythians buried their dead, they took care to provide the corpse with the essentials they thought they needed for the afterlife.

They usually dug a deep hole and built a wooden structure at the bottom. For important people these resembled log cabins that were lined and floored with dark felt – the roofs were covered with layers of larch, birch bark and moss. Inside the tomb, the body was placed in a log trunk coffin, with some of their prized possessions and other objects. Outside the tomb chamber, they placed slaughtered horses, facing east.