Summary: Closing a scalp wound with skin defects is challenging because the scalp skin lacks extensibility and closing it tends to result in a remarkable, widespread, hairless scar. Absorbable symmetric barbed suture device (Stratafix Symmetric; Ethicon, USA) allows wound closure using a pulling motion alone and provides a strong and secure closure for the high-tension area. We used this device to close wide scalp defects easily without tension and with minimized sequential scalp alopecia. The aim of this study was to show our experiences with using this technique. From January 2017 to March 2019, our relaxing suture technique was performed in 7 pediatric patients with scalp alopecia due to various lesions that ranged 23.0 ± 6.5 mm. After resecting the lesions, the galea was sutured using the 3-0 absorbable symmetric barbed suture via a running subcutaneous suture technique. The widespread wound edges were approximated by pulling the suture device. Wound closure was completed with galeal suturing and a superficial suture. We evaluated the width of the postoperative hairless scar at the final follow-up. In all 7 patients, we could approximate the widespread wound edges by pulling alone. Subsequently, the wounds could be closed without tension or difficulty. The mean width of the postoperative hairless scar was 3.3 ± 0.8 mm (range: 1.9–4.3 mm), and no complication was detected during the follow-up period. Our new relaxing suture technique using an absorbable barbed suture with symmetric anchors is a supportive and additional way to help close scalp defects.
Background Postoperative scar adhesions between tendons and phalanx bones cause persistent disability in complex injuries involving tendons and bones of the hand. Although gliding tissue reconstruction is effective in preventing peritendinous adhesion formation and a dorsal digital adipofascial flap is a reliable method to prevent scar adhesion between tendon and bone after extensor tendon repair, no comparative clinical reports exist. This study aimed to determine the usefulness of a gliding tissue reconstruction method by comparing postoperative range of motion between patients who underwent gliding tissue reconstruction and those who did not. Methods Medical records of patients with complex extensor tendon injury who underwent extensor repair between April 2005 and March 2018 were retrospectively analyzed. Ten patients underwent extensor repair with gliding tissue reconstruction using a dorsal digital adipofascial flap and 13 underwent only extensor repair. A triangular flap was separated after zig-zag incision to expose the injured extensor tendon into dermal and adipofascial flaps. The adipofascial flap, based on a dorsal branch of the digital artery, was placed on the injured bone as the tendon gliding surface. The same extensor tendon suture method and rehabilitation protocol were used in both groups. All patients were followed up for 6 to 12 months. Results The mean ± SD % total active movements were 84.1% ± 12.4% and 57.6% ± 13.0% in the groups with and without gliding tissue reconstruction, respectively. Significant differences were found between the 2 groups (P < 0.05). Conclusions Patients with gliding tissue reconstruction had better functional recovery. This reconstruction is recommended to restore the extensor function in cases of complex extensor injury involving finger tendons and bones.
Aims The liver is the major organ shown to remove oxidized low-density lipoprotein (oxLDL) from the circulation. Given increased evidence that thermogenic adipose tissue has anti-atherogenic effects, we used 123I-labeled oxLDL as a tracer to reveal oxLDL accumulation in the brown adipose tissue (BAT) of mice. We also explored the mechanisms of oxLDL accumulation in BAT. Methods and results We used high-resolution nanoSPECT/CT to investigate the tissue distribution of 123I-oxLDL and 123I-LDL (control) following intravenous injection into conscious mice. 123I-oxLDL distribution was discovered in BAT at an intensity equivalent to that in the liver, whereas 123I-LDL was detected mostly in the liver. Consistent with the function of BAT related to sympathetic nerve activity, administering anesthesia in mice almost completely eliminated the accumulation of 123I-oxLDL in BAT, and this effect was reversed by administering β3-agonist. Furthermore, exposing mice to cold stress at 4 °C enhanced 123I-oxLDL accumulation in BAT. Because in 123I-oxLDL, the protein of oxLDL was labeled, we performed additional experiments with DiI-oxLDL in which the lipid phase of oxLDL was fluorescently labeled and observed similar results, suggesting that the whole oxLDL particle was taken up by BAT. To identify the receptor responsible for oxLDL uptake in BAT, we analyzed the expression of known oxLDL receptors (e.g., SR-A, CD36, LOX-1) in cultured brown adipocyte cell line and primary brown adipocytes and found that CD36 was the major receptor expressed. Treatment of cells with CD36 siRNA or CD36 neutralizing antibody significantly inhibited DiI-oxLDL uptake. Finally, CD36 deletion in mice abolished the accumulation of 123I-oxLDL and DiI-oxLDL in BAT, indicating that CD36 is the major receptor for oxLDL in BAT. Conclusion We show novel evidence for the CD36-mediated accumulation of oxLDL in BAT, suggesting that BAT may exert its anti-atherogenic effects by removing atherogenic LDL from the circulation.
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