Highly differentiated follicular carcinoma of ovary (HDFCO) is a rare entity known to arise in struma ovarii. Clinical presentation and radiological features mimic other cystic ovarian neoplasm. Thus, intraoperative diagnosis of this entity can be challenging. We hereby report a HDFCO case of a 52‐year‐old woman, who presented with significant abdominal bloating for 3 months. Imaging showed a 11.7 cm left adnexal‐mixed cystic and solid mass, adhering to the bowel with ascites. The mass was examined intraoperatively and showed multilocular cysts filled with straw or red brown‐colored gelatinous fluid. Microscopically, the tumor consisted of small and large follicles with proteinous material and bland‐looking cuboidal cells, suspicious for struma ovarii or granulosa cell tumor with extensive cystic changes, while imprint cytology slides showed watery colloid with cracking artifact favoring the former. However, the adherence to the bowel suggested HDFCO, and prompted surgical staging. The histology of the ovarian mass in the permanent section resembled goiterous thyroid tissue with invasion of endocervical stroma, uterine wall and colonic serosa, and presence of tumor nodules in omentum leading to the diagnosis of HDFCO. Due to striking resemblance of HDFCO to benign thyroid goiter, searching for invasive and metastatic foci is crucial for correct diagnosis. In addition, intraoperative imprint cytology revealing colloid with cracking artifact is helpful for differentiating struma ovarii and/or HDFCO from other ovarian lesions.

Hyperglycemia is causally related to the vascular complications of diabetes. This patho‐physiological process may be mediated by the activation of protein kinase C (PKC) beta II resulting in an increased oxidative stress and inflammatory response. However, the role of a PKC beta II inhibitor regulating hyperglycemia‐induced endothelial‐leukocyte interactions has not been evaluated in vivo in real‐time. The effect of PKC beta II peptide inhibitor on leukocyte‐endothelial interactions in rat mesenteric postcapillary venule circulation was determined by using intravital microscopy. We found that intraperitoneal injection of 25 mM D‐glucose (2.5 ml, n=6) caused intraperitoneal hyperglycemia and exhibited significantly higher leukocyte rolling, adherence, and transmigration compared to control rats which were intraperitoneal injection of saline (2.5 ml, n=4, P<0.05). By contrast, intraperitoneal injection of D‐glucose with 10 mM PKC beta II inhibitor (12.5 μl, n=3/25.0 μl, n=6) induced the similar intraperitoneal hyperglycemia, but showed significantly less leukocyte‐endothelial interactions compared to D‐glucose injection (P<0.05). In summary, the PKC beta II inhibitor attenuates local hyperglycemia‐induced leukocyte‐endothelial interactions, which may be related to the attenuation of oxidative stress in blood. This study was supported by Center for Chronic Disorders of Aging at PCOM.

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Leukocyte‐endothelial interactions associated with vascular injury are attenuated by endothelial‐derived nitric oxide (NO). Endothelial NO synthase (eNOS) in the presence of tetrahydrobiopterin (BH4) produces NO from L‐arginine and is termed eNOS coupling. However, when the ratio of dihydrobiopterin (BH2) to BH4 is increased, eNOS becomes uncoupled and produces superoxide instead of NO. Protein kinase C epsilon (PKC ε) positively regulates eNOS activity. This study examined modulating eNOS activity and coupling by superfusing BH2 (100 μM) by itself, combined with PKC ε activator (10μM) or PKC ε inhibitor (10μM), or combined with BH4 (100μM) and PKC ε activator in rat mesenteric venules. Intravital microscopy was used to evaluate leukocyte endothelial interactions within a 2 hr period. We found that BH2 (100μM n=3, P<0.05) or combined with PKC ε activator (n=5) significantly increased leukocyte rolling, adherence, and transmigration, compared to Krebs’ buffer controls (n=4, P<0.05). By contrast, the combination of PKC ε activator and BH4 significantly attenuated (n=5, P<0.05) BH2 induced leukocyte rolling/adherence. The BH2 induced response on all three leukocyte endothelial interactions was significantly attenuated by PKC ε inhibitor (n=4 P<0.05). The data suggest that promoting eNOS coupling or inhibiting eNOS uncoupling may be important mechanisms mediating inflammation induced vascular injury. .