This study is to investigate the effect of local phVEGF(165) injection on sciatic nerve regeneration in the rats and to search for a new way in the further treatment of peripheral nerve injuries. Forty-five adult male Wistar rats received a neurotomy to bilateral sciatic nerves, which were subsequently reconnected with 10/0 epineurial nylon sutures. The injured segments was locally injected with normal saline (group A), or 25 microg of phVEGF(165) (group B) or 50 microg phVEGF(165) (group C). Nerve conduction and regeneration were evaluated in terms of the histological changes, weight of gastrocnemius muscles, electrophysiology and morphometric results. Our study demonstrated that rats of group C showed the best results in terms of nerve regeneration, followed by group B and group A. Our findings suggested that local injection of phVEGF165 can facilitate nerve regeneration and promote functional recovery in a dose-dependent manner.

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BackgroundOur routine treatment for ingrown toenail was removal of the surrounding soft tissue and shortening the bone of the distal phalanx. We determined the range and volume of excision based on our experience without an objective standard and routinely performed avulsion of the nail plate.ObjectiveTo take the nail plate as an objective mark during surgical treatment of ingrown toenail to ensure accurate excision.Patients and MethodsFifteen patients with ingrown toenails were treated with this technique. We used the lateral borders of the nail plate as a landmark to determine the volume of soft tissue surrounding the nail plate and distal phalanx to be removed. No avulsion of nail plate was performed.ResultsNo recurrence was observed during the follow-up period, which ranged from 24 to 35 months (29.9 months on average). The visual analog scale for pain showed significant pain relief in the patients. The Vancouver Scar Scale showed acceptable cosmetic outcomes. The width of excised skin ranged from 3.5 to 6.2 mm (5.0 mm on average).ConclusionThe use of the lateral borders of the nail plate as a landmark for surgical intervention of ingrown toenail offered excellent outcomes and reduced loss of healthy tissues.

Activation of PKCβ2 induced by hyperglycemia contributes to impaired angiogenesis in endothelial cells. The purpose of the present study was to investigate whether PKCβ2 inhibition can attenuate the hyperglycemia-induced impaired angiogenesis of myocardium to improve cardiac function following myocardial infarction (MI) in diabetes. In vitro, human umbilical vein endothelial cells (HUVECs) were cultured in low glucose (L-G) (5.6 mmol/l) or high glucose (H-G) (33.3 mmol/l) medium in the presence or absence of LY333531 (LY333) (10 nmol/l), a selective PKCβ2 inhibitor. In vivo, with the use of an MI diabetic rat model, animals were randomized to receive LY333 (10 mg/kg/day) orally for 4 weeks after MI, or no treatment whatsoever. Treatment of HUVECs with LY333 prevented the H-G-induced decrease of tube formation, migration and proliferation. Furthermore, exposure of HUVECs to H-G activated PKCβ2 and decreased levels of phospho-Akt (p-Akt) and phospho-endothelial nitric oxide synthase (p-eNOS) expression, which was also prevented by LY333. Compared with MI rats without therapy, LY333-treated MI rats showed an increase in left ventricular ejection fraction (LVEF) and fractional shortening (FS), but a reduction in infarct size. Furthermore, treatment of rats with LY333 not only significantly increased the capillary density of ischemic myocardium, but also significantly elevated the levels of p-Akt and p-eNOS expression. We also observed a significant increase of VEGF expression in myocardium measured by immunostaining in MI and LY333 groups compared to sham group. Anti-CD31 immunostaining revealed that MI rats treated with LY333 exhibited increased density of capillaries compared with sham group rats. However, treatment of rats with LY333 did not result in significant increases in vascular endothelial growth factor (VEGF) expression at both the mRNA and protein levels in myocardium, and in the plasma level of VEGF compared with MI rats without therapy. Overall, these results suggest that inhibition of PKCβ2 may be a novel therapeutic approach for preserving cardiac function after MI, in part by improving impaired angiogenesis of myocardium in diabetes.