The present study investigated the mechanisms underlying the inhibition of platelet phosphatidylserine (PS) exposure by GPIIb/IIIa blockade. Platelet PS exposure induced by thrombin stimulation was cell-cell contact dependent. GPIIb/IIIa blockade by c7E3 or SR121566 inhibited thrombin-induced platelet PS exposure. Thrombin stimulation induced mild, while A23187 induced extensive platelet-derived microparticle (PDMP) generation. Thrombin-induced PDMP generation was not inhibited by GPIIb/IIIa blockade. Aminophospholipid translocase activity was reduced upon platelet activation by thrombin. The reduction of non-PS-exposing platelets was attenuated by GPIIb/IIIa blockade, while little translocase activity was seen in PS-exposing platelets. Thrombin increased scramblase activity slightly in non-PS-exposing platelets, which was inhibited by GPIIb/IIIa blockade, and markedly enhanced scramblase activity in PS-exposing platelets. Activation of platelet calpain and caspase-3 or cytosolic calcium mobilization were not altered by GPIIb/IIIa inhibition. Thus, GPIIb/IIIa blockade inhibits platelet PS exposure by enhancing translocase activity and attenuating scramblase activity, but does not inhibit PDMP generation.

Despite the numerous flaps for facial reconstruction that have been described, the search for the ideal flap with good color matching and minimal donor-site morbidity continues. In the past 3 years we have repaired 13 facial defects with success using the lateral genicervical flap - a type of facial subdermal vascular network flap (SVNF) - with a pedicle located on the preauricular region. An anatomic study of the facial SVNF, including blood supply and vascular distribution of the face and anatomic characteristics of facial vessels, based on 14 cadaver dissections, was carried out. The blood supply of the facial skin basically originated from the branches of the facial, superficial temporal and infraorbital arteries. The lateral genicervical skin was supplied basically by the branches of the facial, superficial temporal and occipital arteries, but also by the terminal branches of the superior thyroid artery. The branches diverging from these arteries became superficial and formed a subcutaneous arterial network. The arterioles from the network went to the corium layer and formed a subdermal arterial network whose arterioles anastomosed with each other in a honeycomb-like structure. The vascular distribution presented certain directivity on different areas. The blood supply of the pedicle originated from the subdermal vascular network formed by the perforator branches of these arteries. The arterioles from the facial and superficial temporal arteries anastomosed in the lateral genicervical region. From the anatomic study, we think that the viability of the facial SVNF depends basically on the subdermal vascular network formed by the perforator branches of the pedicle, and that the anastomoses between the facial and superficial temporal arteries provide a solid anatomic basis to the lateral genicervical flap. The clinical data also indicated that this flap is a useful alternative for facial, especially superficial temporal, defects. But the directivity must be taken into account in its clinical application.

To cite this article: Reilly S-J, Li N, Liska J, Ekströ m M, Tornvall P. Coronary artery bypass graft surgery up-regulates genes involved in platelet aggregation. J Thromb Haemost 2012; 10: 557-63.

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Gastric cancer is a common malignant tumor in humans. Analysis of clinical data of gastric cancer revealed that adhesion G protein-coupled receptor G2 (ADGRG2), endoplasmic reticulum oxidoreductase 1β, lactate dehydrogenase B and chromosome 1 open reading frame 115 were abnormally highly expressed in gastric cancer. ADGRG2 was not only highly expressed in gastric cancer tissues, but was also associated with poor prognosis in patients with gastric cancer. Numerous oncogenes and tumor suppressor genes are directly involved in the regulation of the cell cycle. ADGRG2 was shown to promote cell proliferation by promoting the G1/S transition. ADGRG2 did not affect the expression of CDK4 or cyclin D1 (CCND1), but was found to affect the cell cycle by promoting the formation of the cell cycle-dependent complex CDK4/CCND1, thereby promoting cell proliferation, and affecting the formation and development of gastric cancer.

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