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The chiasmal and subchiasmal surfaces are of critical importance in connection with the performance of surgical procedures owing to the critical blood supply to these areas. Recently, the perforating arteries providing the blood to the optic nerves and chiasm have gained attention as they significantly affect the morbidity from surgical approaches. Intraoperative preservation of these perforating arteries is considered critical to prevent further visual loss. Thirty autopsy specimens, including the optic apparatus, were examined for their perforating arteries feeding the optic chiasm and optic nerves. The optic nerves and chiasmal surfaces were divided into four zones based on the presence and numbers of perforating arteries as anterior superior-posterior superior surfaces and anterior inferior-posterior inferior surfaces. The superior surface of the optic chiasm was supplied by the A1 segments of the bilateral anterior cerebral arteries and by the perforating arteries originating from the anterior communicating artery. On the other hand, the inferior surface of the optic chiasm was fed by the bilateral posterior communicating arteries and by the supraclinoidal segments of the bilateral carotid arteries. We demonstrated the anatomical involvement of a large number of nourishing arteries in feeding the optic apparatus related to the perforating arteries by classifying them into zones based on the surgical approaches, which has been rarely reported in the literature.Knowledge of the anatomic variations in the pectineus muscle is important for vascular surgeons to minimize complications following surgical approach to the distal part of the deep femoral artery. During routine dissection of the thigh, variations in the bilateral pectineus muscles were identified in an 82-year-old male cadaver. On both sides, the superficial and deep layers of the pectineus were divided at its distal part, forming a triangular-shaped hiatus between them and the femur shaft. Distally, the tendon of the superficial part intermingled with the tendon of the adductor longus. The tendon of the deep part was inserted into the pectineal line. On the right side, the deep femoral artery and its first perforating artery passed through the hiatus. On the left side, the deep femoral artery pierced the hiatus, and then, the first perforating artery was branched from the deep femoral artery. No reported case has described a pectineal hiatus. The variations observed in this study are an ontogenetic vestige of the two different origins of the pectineus. The insertion of the superficial layer into the adductor longus tendon suggests a close relationship between these muscles during prenatal development. Surgeons should be aware of the variation to minimize injury to the pectineus muscle while approaching the deep femoral artery.Nasopharyngeal carcinoma is a type of otolaryngological malignancy with high incidence. selleck products Long non-coding RNAs (lncRNAs) are closely related to nasopharyngeal carcinoma. LncRNA AFAP1-AS1 (AFAP1-AS1) has been found to play important roles in nasopharyngeal carcinoma progression and poor prognosis. However, the mechanism underlying AFAP1-AS1 in regulating nasopharyngeal carcinoma is still unclear. In current study, AFAP1-AS1 was found to be up-regulated in nasopharyngeal carcinoma tissues and cells. AFAP1-AS1 overexpression and knockdown were conducted in nasopharyngeal carcinoma cells. The results proved that AFAP1-AS1 promoted the survival and migration of nasopharyngeal carcinoma cells. Additionally, specificity protein 1 (SP1) was enhanced in nasopharyngeal carcinoma tissues and cells, and induced AFAP1-AS1 expression. The interaction between AFAP1-AS1 and miR-497-5p was confirmed. AFAP1-AS1 was demonstrated to regulate CELF1, a target gene of miR-497-5p. Further functional analysis revealed that AFAP1-AS1 knockdown attenuated SP1-induced nasopharyngeal carcinoma progression. These results indicate that SP1-induced AFAP1-AS1 facilitates nasopharyngeal carcinoma progression by regulating miR-497-5p/CELF1 pathway, which provides a new target for nasopharyngeal carcinoma treatment.Ovarian cancer (OC) is a highly malignant tumor. X inactive specific transcript (XIST) was identified as a cancer-related gene, while its therapeutic effect in OC was poorly defined. The present study was designed to investigate the effectual corollary of the lncRNA XIST in OC. RT-qPCR was used to detect the XIST and miR-106a expression levels of OC tissues and cell lines. OC cell apoptosis and proliferation were detected by flow cytometry, colony formation, and CCK-8 assays. Moreover, bioinformatics analysis was used to predict the targeted miRNA of XIST. The dual-luciferase reporter and RNA pull-down assays were then used to verify the interaction between miR-106a and XIST. OC xenograft nude mice were raised to measure tumor growth. Notably, OC tissues and cells exhibited low XIST levels and high miR-106a levels. The XIST upregulation decreased the OVCAR3 and CAOV3 cell proliferation and inversely promoted cell apoptosis. miR-106a targeted the XIST. Also, the miR-106a overexpression reversed the inhibitory effects of XIST on OC cell proliferation and apoptosis. Our in vivo results suggested that XIST was involved in tumor growth deceleration, while the miR-106a reversed the effect. To conclusion, the present study demonstrated that XIST suppressed OC development via sponging miR-106a both in vitro and in vivo.MAFG-AS1 is an oncogenic lncRNA in multiple types of cancer. However, its role in bladder cancer (BC) remains unclear. The present study aimed to investigate the function of MAFG-AS1 in BC. BC and paired non-tumor tissues were collected. Two BC cell lines HT01197 and HT-1376 were used. Dual luciferase activity assay, RT-qPCR, western blot, CCK-8, transwell invasion assay, and wound healing assay were performed. We found that MAFG-AS1 was significantly up-regulated in BC tissues and predicted a poor survival rate. MAFG-AS1 interacted with miR-125b-5p. However, the expression levels of MAFG‑AS1 and miR-125b-5p were not obviously correlated in BC tissues, and MAFG‑AS1 and miR-125b-5p did not regulate the expression of each other. Interestingly, we found that SphK1, a downstream target of miR-125b-5p, was negatively correlated with miR-125b-5p, while it was positively correlated with MAFG-AS1 across BC tissues. In addition, overexpression of MAFG‑AS1 upregulated the expression of SphK1 in BC cells, and attenuated the inhibitory effects of miR-125b-5p on the expression of SphK1.
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