Brachydactyly, is a medical term which means "shortness of the fingers and toes". The shortness is relative to other parts of the body. Brachydactyly is an inherited dominant trait, it most occurs as an isolated dysmelia, but can occur with other anomalies as part of many congenital syndromes. Brachydactyly can be a signal that one will be at risk for heart problems as they age. Nomograms for normal values of finger length as a ratio to other body measurements have been published. In clinical genetics the most used index of digit length is the dimensionless ratio of the length of the 3rd finger to the hand length. Both are expressed in the same units and are measured in an open hand from the fingertip to the principal creases where the finger joins the palm and where the palm joins the wrist. There are several types of Brachydactyly: In the above brachydactyly syndromes, short digits are the most prominent of the anomalies, but in many other syndromes, brachydactyly is a minor feature compared to the other anomalies or problems comprising the syndrome.

Clubbed thumb Syndactyly Type A2 Brachydactyly type A1 at NIH's Office of Rare Diseases Brachydactyly type A2 at NIH's Office of Rare Diseases Brachydactyly type A3 at NIH's Office of Rare Diseases Brachydactyly type A6 at NIH's Office of Rare Diseases Brachydactyly type A7 at NIH's Office of Rare Diseases Brachydactyly type B at NIH's Office of Rare Diseases Brachydactyly type C at NIH's Office of Rare Diseases Brachydactyly type E at NIH's Office of Rare Diseases Brachydactyly types B and E combined at NIH's Office of Rare Diseases

The 2006 World Touring Car Championship season was the third season of FIA World Touring Car Championship motor racing. It featured a ten event, twenty race series which commenced on 2 April 2006 and ended on 19 November; the series was open to Super 2000, Diesel 2000 and Super Production Cars, with two titles awarded, the FIA World Touring Car Champion for Drivers and the FIA World Touring Car Champion for Manufacturers. Andy Priaulx won BMW won the Manufacturers award; the following drivers and teams contested the 2006 World Touring Car Championship. Changed Teams Gabriele Tarquini: Alfa Romeo Racing Team → SEAT Sport James Thompson: Alfa Romeo Racing Team → SEAT SportEntering WTCC including those who entered one-off rounds in 2005 Yvan Muller: British Touring Car Championship → SEAT Sport Marcel Costa: No full-time drive → BMW Team Italy-Spain Gianni Morbidelli: FIA GT Championship → N-Technology Salvatore Tavano: Italian Superturismo Championship → N-Technology Maurizio Ceresoli: Italian Formula Three Championship → GR Asia Pierre-Yves Corthals: No full-time drive → Jas Motorsport Ryan Sharp: Formula Renault 3.5 Series → Jas Motorsport Luca Rangoni: No full-time drive → Proteam Motorsport Emmet O'Brien: European Alfa Romeo 147 Challenge → Wiechers-Sport Diego Romanini: FIA GT Championship → Wiechers-SportLeaving WTCC Fabrizio Giovanardi: Alfa Romeo Racing Team → British Touring Car Championship Antonio García: BMW Team Italy-Spain → No full-time drive Thomas Klenke: Ford Hotfiel Sport → No full-time drive Michael Funke: Ford Hotfiel Sport → ADAC GT Masters Roberto Colciago: Jas Motorsport → Italian Superturismo Championship Adriano de Micheli: Jas Motorsport → No full-time drive Giuseppe Cirò: Proteam Motorsport → Ferrari Challenge Marc Hennerici: Wiechers-Sport → Veranstaltergemeinschaft Langstreckenpokal Nürburgring Each event comprised two races of 50 kilometres distance.

The starting grid for the first race was determined by the results of the qualifying session and the grid for the second race by the provisional results of the first race, with the top eight positions reversed. Championship points were awarded on a 10–8–6–5–4–3–2–1 basis for the first eight positions in each race. † — Drivers did not finish the race, but were classified as they completed over 90% of the race distance. Championship points were awarded on a 10–8–6–5–4–3–2–1 basis for the first eight positions in each race. However, only the two best placed cars per manufacturer were eligible to score points and all other cars from that manufacturer were considered invisible as far as point scoring was concerned. Points were awarded on a 10–8–6–5–4–3–2–1 basis for the first eight finishers of those entries which were classified as Independents. Dead-heat10p: 14th Edman, 15th A. Chi Hong 5p: 17th L. Molo, 18th O. Hidalgo 2p: 21st M. De Villota, 22nd P. Geipel, 23rd D. Roda, 24th S. Valli Points were awarded on a 10–8–6–5–4–3–2–1 basis for the first eight finishers of those entries which were classified as Independents.

FIA World Touring Car Championship official website as archived at web.archive.org on 23 December 2006

The type II and XI collagenopathies are a group of disorders that affect connective tissue, the tissue that supports the body's joints and organs. These disorders are caused by defects in type XI collagen. Collagens are complex molecules that provide structure and elasticity to connective tissue. Type II and type XI collagen disorders are grouped together because both types of collagen are components of the cartilage found in joints and the spinal column, the inner ear, the jelly-like substance that fills the eyeball; the type II and XI collagenopathies result in similar clinical features. Genetic changes are related to the following types of collagenopathy, types II and XI; the system for classifying collagenopathies is changing as researchers learn more about the genetic causes of these disorders. The clinical features of the type II and XI collagenopathies vary among the disorders, but there is considerable overlap. Common signs and symptoms include problems with bone development that can result in short stature, enlarged joints, spinal curvature, arthritis at a young age.

For some people, bone changes can be seen only on X-ray images. Problems with vision and hearing, as well as a cleft palate with a small lower jaw, are common; some individuals with these disorders have distinctive facial features such as protruding eyes and a flat nasal bridge. Mutations in the COL11A1, COL11A2, COL2A1 genes cause collagenopathy, types II and XI; these genes carry instructions for the protein strands that make up type type XI collagen. All collagen molecules are made of three protein strands; the alpha chains may be different, depending on the type of collagen. Type II collagen is made by combining three copies of the alpha chain made by the COL2A1 gene. Type XI collagen, on the other hand, is composed of three different alpha chains: the products of the COL2A1, COL11A1, COL11A2 genes. Mutations in these genes interfere with the proper assembly of type II and XI collagens or reduce the amount of these collagens. Defective or reduced numbers of collagen molecules affect the development of bones and other connective tissues, causing the signs and symptoms of the type II and XI collagenopathies.

This article incorporates public domain text from The U. S. National Library of Medicine