Entire A2 Research Articles

Recent evolutions in flexor tendon repairs and rehabilitation.

This article reviews some recent advancements in repair and rehabilitation of the flexor tendons. These include placing sparse or no peripheral suture when the core suture is strong and sufficiently tensioned, allowing the repair site to be slightly bulky, aggressively releasing the pulleys (including the entire A2 pulley or both the A3 and A4 pulleys when necessary), placing a shorter splint with less restricted wrist positioning, and allowing out-of-splint active motion. The reported outcomes have been favourable with few or no repair ruptures and no function-disturbing tendon bowstringing. These changes favour easier surgeries. The recent reports have cause to re-evaluate long-held guidelines of a non-bulky repair site and the necessity of a standard peripheral suture. Emerging understanding posits that minor clinically noticeable tendon bowstringing does not affect hand function, and that free wrist positioning and out-of-splint motion are safe when strong surgical repairs are used and the pulleys are properly released.

Commentaries on Clinical results of releasing the entire A2 pulley after flexor tendon repair in zone 2C. K. Moriya, T. Yoshizu, N. Tsubokawa, H. Narisawa, K. Hara and Y. Maki. J Hand Surg Eur. 2016, 41: 822-28.

Commentaries on Clinical results of releasing the entire A2 pulley after flexor tendon repair in zone 2C. K. Moriya, T. Yoshizu, N. Tsubokawa, H. Narisawa, K. Hara and Y. Maki. J Hand Surg Eur. 2016, 41: 822-28.

Clinical results of releasing the entire A2 pulley after flexor tendon repair in zone 2C.

We report the results of complete release of the entire A2 pulley after zone 2C flexor tendon repair followed by early postoperative active mobilization in seven fingers and their comparisons with 33 fingers with partial A2 pulley release. In seven fingers, release of the entire A2 pulley was necessary to allow free gliding of the repairs in five fingers and complete release of both the A2 and C1 pulleys was necessary in two. No bowstringing was clinically evident in any finger. Two fingers required tenolysis. Using Tang's criteria, the function of two digits was ranked as excellent, four good and one fair; there was no failure. The functional return in these seven fingers was similar with that in 33 fingers with partial A2 pulley release; in these patients only one finger required tenolysis. Our results support the suggestion that release of the entire A2 pulley together with the adjacent C1 pulley does not clinically affect finger motion or cause tendon bowstringing, provided that the other pulleys are left intact. IV.

Giant heterogeneous magnetostriction in Fe–Ga alloys: Effect of trace element doping

Enhanced magnetostriction in iron-rich Fe–Ga alloys has been attributed to a heterogeneous nanostructure with tetragonal inclusions, although direct experimental evidence for their structure was lacking. Here we use transmission electron microscopy to show that melt-spun, (001) textured Fe83Ga17 ribbons contain 3 nm inclusions with c-axis Ga–Ga pairs aligned in a tetragonal L60-type structure; the induced tetragonality of the entire A2 matrix is observed directly by synchrotron X-ray diffraction. Trace doping with 0.2 atomic % nonmagnetic elements such as La or Pb increases the magnetocrystalline anisotropy and greatly enhances the magnetostriction. Rare-earth dopants from La to Lu produce a quarter-shell variation of the magnetic anisotropy; the crystal field parameter A20 is determined to be −15 Ka0−2. The best trace dopants are the light rare earths Ce and Pr that give a transverse magnetostriction of up to −800 ppm, as these elements soften the tetragonal modulus via their crystal field interaction. A new model is proposed to explain nanoheterogeneous magnetostriction, where the Ga–Ga pairs remain fixed, but the tetragonal axis of the matrix can be realigned in a magnetic field by a series of small deformations of the A2 matrix. These results signal a new approach to creating highly-magnetostrictive materials.

The diversity of the immune response to the A2 domain of human factor VIII

AbstractApproximately 30% of patients with severe hemophilia A develop inhibitory anti–factor VIII (fVIII) antibodies (Abs). We characterized 29 anti-human A2 monoclonal Abs (mAbs) produced in a murine hemophilia A model. A basis set of nonoverlapping mAbs was defined by competition enzyme-linked immunosorbent assay, producing 5 major groups. The overlapping epitopes covered nearly the entire A2 surface when mapped by homolog-scanning mutagenesis. Most group A mAbs recognized a previously described epitope bounded by Arg484-Ile508 in the N-terminal A2 subdomain, resulting in binding to activated fVIII and noncompetitive inhibition of the intrinsic fXase complex. Group B and C mAbs displayed little or no inhibitory activity. Group D and E mAbs recognized epitopes in the C-terminal A2 subdomain. A subset of group D mAbs inhibited the activation of fVIII by interfering with thrombin-catalyzed cleavage at Arg372 at the A1-A2 domain junction. Other group D mAbs displayed indeterminate or no inhibitory activity despite inhibiting cleavage at Arg740 at the A2-B domain junction. Group E mAbs inhibited fVIII light-chain cleavage at Arg1689. Inhibition of cleavages at Arg372 and Arg1689 represent novel mechanisms of inhibitor function and, along with the extensive epitope spectrum identified in this study, reveal hitherto unrecognized complexity in the immune response to fVIII.

Primary Pulley Enlargement in Zone 2 by Incision and Repair With an Extensor Retinaculum Graft

This retrospective study documents the results of primary enlargement of tendon sheath pulleys by incision and extensor retinaculum graft repair during flexor tendon repairs in zone 2 in 9 fingers. The entire A2 or A4 pulley was enlarged by complete incision and repaired with an interposed extensor retinaculum graft at the time of primary flexor tendon repair in a total of 9 fingers in 7 patients, ages 15 to 54 years. The indication for primary pulley enlargement was failure of the tendon repair to glide smoothly and without snagging through the normally tight-fitting pulley system. In no case was more than one major pulley enlarged, and the entire A1 pulley was never enlarged. The zone 2 tendon repairs were done using a 2-strand modified Kessler 3-0 core suture and a 6-0 nylon running circumferential suture. The follow-up averaged 3.6 years. Interphalangeal total active motion and Strickland-Glogovac grade in patients with adequate follow-up of more than 6 months or obtaining full range of motion were obtained from a retrospective chart review. Interphalangeal total active motion averaged 127 degrees and the scores according to the Strickland-Glogovac system were excellent for 3, good for 2, fair for 2, and poor for 2. There were no tendon ruptures. Two fingers in one patient required a tenolysis and a third finger had secondary skin scar lengthening. Two fingers had visible and palpable bowstringing when seen at long-term follow-up and there was an average flexion contracture of 21 degrees. Primary pulley enlargement using a free graft in zone 2 tendon injuries may achieve the 3 goals of providing a good gliding environment, avoiding triggering, and minimizing bowstringing. These initial clinical outcomes are average for zone 2 tendon repair, but encouraging. Further research and refinement in surgical technique and rehabilitation method are needed to minimize flexion contractures.

Sedimentary Processes of the Qingdao Nearshore Traced Using a Multi-radionuclide Approach

Sediment cores were collected from two sites (A2 and ZQ) in the Qingdao sea area of the Yellow Sea. Radionuclides 40K, 137Cs, 210Pb, 226Ra, 228Ra, 228Th, 234Th, and 238U in the cores were measured using HPGe γ spectrometry. The sedimentation rate of the A2 Core using 210Pbex and 137Cs was 0.665 cm yr−1, therefore this 32 cm long core represents a 48 year timespan leading to the sampling date in 2001. The mixing layer was restricted to the upper 5 cm as determined from the profile of 234Th. The uniformity of the activity distributions of 40K and 238U throughout the A2 Core and the activity distributions of 226Ra, 228Ra and 228Th below the mixing layer suggested that no significant oceanographic event or change in sediment material source had occurred during this timespan. The 210 Pb was in excess relative to 226Ra, but 226Ra was deficient with respect to 238U in the entire A2 Core, while excess 234Th and 228Th were apparent only in the surface 5 cm. Total organic matter (TOM) in Core A2 decreases with depth. The second core, taken to a depth of 14 cm, was from Site ZQ, which is located near Zhanqiao, Qingdao. The variations of the nuclide activity ratios in this core were similar to those in the A2 Core, i.e., the excess 210 Pb and 226Ra deficiency were consistent throughout the core but excess 228Th was only in the surface to a depth of 2 cm. The 40K activity in the ZQ Core fluctuated and showed no real trend with depth. The activities of 137Cs, 210Pb, 226Ra and 238U in the entire length of Core ZQ, and 228Ra and 228Th from 2 cm to the bottom, were comparable within the uncertainty of measured activity.

Activated Protein C Cleavage of Factor Va Leads to Dissociation of the A2 Domain

The products of cleavage of bovine factor Va by activated protein C (APC) in the presence and absence of phospholipid (25% phosphatidylserine, 75% phosphatidylcholine, PCPS) were evaluated using sedimentation velocity/equilibrium methods in the analytical ultracentrifuge and by immunoprecipitation using an antibody directed against the light chain of the factor Va molecule. The molecular weight and sedimentation coefficient of the associated heavy and light chains of factor Va, 173,000 (7.9 S) is reduced to 132,000 (7.1 S) by APC cleavage at Arg505 and Arg662. Complete cleavage of the factor Va heavy chain (with APC-PCPS) at Arg505, Arg662 and Arg306 results in a drastic change in the molecular weight observed for the product. Two products are resolved with sedimentation coefficients of 3.3 and 6.3 S with estimated molecular weights of 48,000 and 114,000, respectively. Immunoprecipitation studies showed that the products of factor Va cleavage at Arg505 and Arg662 (A1A2N.A2C.LC) are mostly noncovalently associated and consequently immunoprecipitated with an antibody directed against the light chain of the factor Va molecule. In contrast, for factor Va cleaved at Arg505, Arg662, and Arg306 the precipitated complex consisted of the A1 domain (residues 1-306) and the light chain (residues 1537-2183) of factor Va (A1.LC). The fragments corresponding to residues 307-505 (A2N) and 506-662 (A2C) are found in the supernatant. The combined mass of these two products (48,000) is similar to the estimated mass of the 3.3 S fragment estimated from sedimentation velocity/equilibrium studies; while the combined mass of the 1-306 + 1537-2183 products corresponds to 114,000, the estimated mass of the 6.3 S fragment. These data lead to the conclusion that cleavages at Arg306, Arg505, and Arg662 of the factor Va molecule resulted in the dissociation of the entire A2 domain as two noncovalently associated fragments (A2N.A2C). Enzyme kinetic and light scattering data suggest that the complete inactivation of the factor Va molecule involves not only cleavage at Arg306 but also the dissociation of the A2 domain. These data also suggest that the complete APC inactivation of the factor Va molecule is analogous to the spontaneous inactivation of factor VIIIa, which occurs via the dissociation of the A2 domain.