Congenital dysplasia involving both medial and inferior recti: clinical features and surgical outcomes.

AIM: To investigate the clinical features and surgical outcomes of congenital dysplasia involving both inferior recti (IR) and medial recti (MR) muscles. METHODS: A retrospective review was conducted including cases of simultaneous congenital dysplasia of IR and MR that were diagnosed and surgically treated at the Zhongshan Ophthalmic Center, Sun Yat-sen University, China, from July 2009 to November 2019. Ocular motility, ocular alignment at distance (6 m) and near (33 cm) by prism alternating cover test and stereoacuity were assessed in all patients before and after surgery. RESULTS: A total of five patients (four males and one female; three with right eye and two with left eye congenital dysplasia) were included in this review. The patients ranged in age from 10 to 42y (21±13.4y). The main clinical findings were hypertropia and exotropia of the affected eye, along with motility limitations in adduction and depression. Lateral rectus (LR) recession/transposition combined with IR resection was performed in one case. Two scheduled surgeries were performed in four cases, with one involving superior rectus recession and IR resection and the others LR recession and MR resection. Mean±SD pre-surgical exotropia of 51.0±31.11 prism diopter (PD) and hypertropia of 29.20±7.12 PD in the primary position were decreased to 3.6±12.90 and 3.2±10.09 PD, respectively, at two years after surgery, with a success rate of 60% and an under-correction rate of 40%. CONCLUSION: The main clinical features associated with simultaneous MR/IR congenital dysplasia are hypertropia and exotropia of the affected eye along with motility limitations in adduction and depression. Scheduled two-stage surgeries achieved a success rate of 60%.

Congenital ocular counter-roll: a review of cases treated exclusively by ophthalmologists.

AIM: To review the demographics, clinical manifestations, and surgical experiences of patients with congenital ocular counter-roll, whose treatments were performed exclusively by ophthalmologists. METHODS: A retrospective review was conducted consisting of patients who received strabismus surgery between 2017 to 2019. Patients with obvious ocular counter-roll were included. RESULTS: A total of 7008 patients who received strabismus surgery, 28 (12 males, 16 females) were diagnosed as congenital ocular counter-roll, accounting for 0.40%. All patients were initially misdiagnosed: 21 patients were misdiagnosed as superior oblique palsy (SOP), 3 as inferior oblique overaction, 2 as dissociated vertical deviation (DVD), 1 as superior oblique overaction with A-pattern exotropia, and 1 as medial rectus palsy. The mean±SD age was 12.4±9.4y (range 2.5-36y). The most common clinical findings included ocular counter-roll, vertical deviation or vertical deviation combined with outward deviation and head tilt. At follow-up, an excellent surgical result was achieved in 20 patients. Preoperative horizontal deviation of 26±24 prism diopter (PD) and vertical deviation of 18±12 PD were reduced to 0±12 PD (P=0.0001) and 3±4 PD (P=0.001), respectively. CONCLUSION: Congenital ocular counter-roll is a rare supranuclear vertical strabismus caused by congenital abnormalities involving vestibule-ocular reflex pathways. In addition to ocular counter-roll, the most salient clinical features included, but are not limited to, hyperdeviation, outward deviation, overelevation in adduction and head tilt.

Enhanced 5-fluorouracil cytotoxicity in high COX-2 expressing hepatocellular carcinoma cells by wogonin via the PI3K/Akt pathway.

Combination therapies may increase the antitumor effects and reduce the adverse effects for the treatment of hepatocellular carcinoma. In this study, we determined the effects of 5-fluorouracil alone or in combination with wogonin in vitro and in vivo, and we investigated the possible mechanisms. The combination of these 2 drugs led to a decrease in survival and a significant synergistic inhibitory effect on high COX-2 expression in SMMC-7721 hepatocellular carcinoma (HCC) cells. Furthermore, the results show that this combination inhibits COX-2 expression and increases sensitivity to chemotherapeutic agents partly through regulating the PI3K/Akt signaling pathway. Moreover, the combination treatment caused a significant growth inhibition of human tumor xenografts in vivo. In conclusion, wogonin may increase the cytotoxicity of some antineoplastic agents and it can be used in combination with these agents as a novel therapeutic regimen for HCC treatment.

Oroxylin A improves the sensitivity of HT-29 human colon cancer cells to 5-FU through modulation of the COX-2 signaling pathway.

5-Fluorouracil (5-FU) is a principal drug for the treatment of colorectal cancer. Due to its low response and high toxicity, synergistic effects of 5-FU in combination with other drugs have been widely researched. This study investigated whether oroxylin A improved the sensitivity of HT-29 human colon cancer cells to 5-FU. A correlation between COX-2 inhibition by oroxylin A and a synergistic effect of 5-FU on the growth of HT-29 cells was observed, and a COX-2 pathway for this effect was recognized; oroxylin A evidently elevated the level of reactive oxygen species in HT-29 cells, which subsequently inhibited COX-2 expression and enhanced the susceptibility of HT-29 cells to 5-FU. Likely also related to COX-2 inhibition, oroxylin A decreased PGE(2) levels in HT-29 cells. The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells. Ultimately, a combination of 5-FU with oroxylin A significantly reduced the growth of HT-29 tumors in nude mice compared with treatment with 5-FU or oroxylin A alone. In conclusion, a combination of 5-FU and oroxylin A has a significant synergistic effect in the inhibition of HT-29 cell proliferation in vitro and controls HT-29 tumor growth in vivo. This synergistic effect may be mainly related to COX-2 inhibition by oroxylin A in HT-29 cells.