The arterial source of the flap,the anastomoses of cutaneous arteries in theskin and subcutaneous tissue and nervous distribution in the flap were observed andsurveyed in 42 upper limbs of adult cadavers.1.The arterial source of the flap comes mainly from the cutaneous branches ofprofund brachial artery,radial collateral artery,lateral humeral cutaneous artery andcutaneous branches of the posterior circumflex humeral artery.In most cases theprofund brachial artery and radial collateral artery may be served as the vascularpedicle of the flap of lateral brachium in transplantation.2.The cutaneous arteries in this flap anastomose each other to from a networkin the skin and subcutaneous tissue.Cutaneous arteries arising from the medial brac-hial region and the upper part of forearm also participate in the formation of thisvascular network.3.The veins of the flap contain both superficial and deep groups:The superfi-cial group is the cephalic vein of brachium which goes upward along the lateralsulcus of m.biceps brachii and its outer caliber is somewhat wider;the deep groupfollows the profund brachial artery or radial collateral artery as their venae comit-antes.Both groups may be sutured together or separately with veins of the recipientin skin grafting.4.The lateral brachial cutaneous nerve and posterior antebrachial cutaneousnerve pierce through the lateral intermuscular septum at various levels,and innervateover the skin in lateral brachial and posterior forearm regions.Since the posteriorbrachial cutaneous nerve is accompanied closely by the radial collateral artery,muchattention should be paid to it in cutting skin flap.5.The extent of cutting a skin flap in lateral brachial region can be enlargeddue to free anastomoses with arteries of adjacent regions which was demonstrated byperfusing red ink into profund brachial artery.The flap of lateral brachium maybe subdivided into following three parts:the upper,middle and lower,the vascularpedicle of which are the cutaneous branch of posterior circumflex humeral artery,lateral humeral cutaneous artery and profund brachial artery(or radial collateralartery)respectively.

The cutaneous arteries of the forearm and their anastomoses in skin and subcutaneous tissue were invetigated on 35 upper limbs.1. The average length of the radial artery is 215.3 mm. This artery can be divided into a covered part and a exposed part. Their lengths are 117.7 mm. and 101.4 mm. respectively. The calibers of the upper end, the intermediate point, and the lower end of the radial artery are 2.7mm, 2.3 mm and 2.4 mm respectively.2. The exposed part of the radial artery sends out more cutaneous branches (9.6 branches) than the covered part (4.2 branches), While their muscular branches are nearly equal in number. The calibers of the cutaneous and muscular branches of the radial artery varies from 0.3～0.5 mm.The fine anastomoses of the cutaneous branches exist between the radial and ulnar arteries and between the radial and ulnar arteries and the dorsal interosseus artery and they form an arterial networks in the subcutaneous tissue of the whole forearm. For blood supply a skin flap may be cut from the whole forearm from the standpoint of morphology.4. The calibers of the radial and cephalic veins at the level of middle part of the forearm are 1.3 mm and 2.8 mm respectively. As the vasular pedicle both the veins should be anastomosed during transplant operation in order to increase the volume of the draining blood.5. The skin flap of forearm blongs to a type of blood supply of arterial trunk network, which have been distinguished with that of some other skin and myocutaneous flaps according to the anatomical characteristics of the radial artery.

Objective:To investigate the pathogenic gene of the two pedigrees with hereditary synpolydactyly.Methods:Clinical data of two families admitted to the Linyi People’s Hospital due to hereditary synpolydactyly in January 2019 and December 2020 were recruited. Peripheral blood samples were collected and genomic DNAs were extracted. Whole exome sequencing was conducted to detect the pathological mutations and Sanger sequencing was used to verify the variants. The pathogenicity of the mutations was predicted according to PolyPhen-2, PROVEAN and the American College of Medical Genetics and Genomics (ACMG) guidelines.Results:There were a total of 5 patients (2 males and 3 females) in family 1. The proband was an 8-year-old girl, showed syndactyly of the third and fourth fingers of the right hand with webbed fusion and distal fingernail fusion. The rest of the fingers and feet were normal. There were a total of 4 patients (all females) in family 2. The proband was a 4-year-old girl, and showed the interlocking of the third and fourth fingers on both hands and the lateral curvature of the indicator finger. Two mutations of the homeobox D13(HOXD13) gene, c. 917G>A and c. 917G>T were detected and co-segregated with the disease phenotype in two affected families. Moreover, the variant of c. 917G>T is a novel missense mutation of the HOXD13 gene. According to ACMG guidelines, c. 917G>A meets the criteria of pathogenic variation (PS1+ PS4+ PM1+ PM2+ PP3) and c. 917G>T meets the criteria of likely pathogenic variation (PM2+ PM5+ PP3+ PP4).Conclusion:The HOXD13 gene c. 917G>A and c. 917G>T mutations are identified to be responsible for hereditary synpolydactyly in these two families.

Objective:To investigate the pathogenic gene of the two pedigrees with hereditary synpolydactyly.Methods:Clinical data of two families admitted to the Linyi People’s Hospital due to hereditary synpolydactyly in January 2019 and December 2020 were recruited. Peripheral blood samples were collected and genomic DNAs were extracted. Whole exome sequencing was conducted to detect the pathological mutations and Sanger sequencing was used to verify the variants. The pathogenicity of the mutations was predicted according to PolyPhen-2, PROVEAN and the American College of Medical Genetics and Genomics (ACMG) guidelines.Results:There were a total of 5 patients (2 males and 3 females) in family 1. The proband was an 8-year-old girl, showed syndactyly of the third and fourth fingers of the right hand with webbed fusion and distal fingernail fusion. The rest of the fingers and feet were normal. There were a total of 4 patients (all females) in family 2. The proband was a 4-year-old girl, and showed the interlocking of the third and fourth fingers on both hands and the lateral curvature of the indicator finger. Two mutations of the homeobox D13(HOXD13) gene, c. 917G>A and c. 917G>T were detected and co-segregated with the disease phenotype in two affected families. Moreover, the variant of c. 917G>T is a novel missense mutation of the HOXD13 gene. According to ACMG guidelines, c. 917G>A meets the criteria of pathogenic variation (PS1+ PS4+ PM1+ PM2+ PP3) and c. 917G>T meets the criteria of likely pathogenic variation (PM2+ PM5+ PP3+ PP4).Conclusion:The HOXD13 gene c. 917G>A and c. 917G>T mutations are identified to be responsible for hereditary synpolydactyly in these two families.