Delayed presentation of a right congenital diaphragmatic hernia following left congenital diaphragmatic hernia repair in infancy.

INTRODUCTION AND IMPORTANCE: Congenital diaphragmatic hernias (CDH) affect variable portions of diaphragm, resulting in herniation of abdominal contents into the chest. CDH typically is diagnosed prenatally or presents soon after birth with respiratory distress and abnormal chest X-ray (CXR) findings. Presentation after infancy is rare but well described. We present a case of delayed presentation of a right CDH following left CDH repair. CASE PRESENTATION: An 18-month-old boy with a history of a left CDH repaired in the newborn period presented with a newly elevated right hemidiaphragm presumed to be an eventration. He re-presented 9 months later with abdominal pain and respiratory distress. Xray was concerning for gastric volvulus within the right chest. Surgical exploration revealed a small right sided diaphragmatic hernia with an incarcerated liver and stomach. This was repaired without event. CLINICAL DISCUSSION: Normal appearing CXR following L CDH repair led to delayed recognition of this right CDH. Delayed presentation was likely due to the liver covering the small diaphragmatic defect, preventing early migration of the intra-abdominal viscera into the chest. Recurrence of the CDH is the most common cause of respiratory and gastrointestinal symptoms following prior repair, but an unrecognized contralateral defect is a rare possibility. CONCLUSION: In a patient with a prior history of a left CDH who presents with respiratory and gastrointestinal symptoms, along with a recurrence of the left sided CDH, the presence of a right sided defect should be considered if the right hemidiaphragm is newly elevated.

Relationship between contrast sensitivity and corneal shape following overnight orthokeratology.

AIM: To evaluate the relationship between contrast sensitivity (CS) and corneal shape following overnight orthokeratology (OK). METHODS: We conducted a retrospective clinical study of 80 lens-wearing myopia patients, all of whom had undergone OK and had been evaluated by Orbscan II topography. We measured the surface irregularity index (SIRI) of corneal topography at 3 and 5 mm, the size of the flattened central corneal curvature of OK lens (zone A), the size of the cornea altered by OK lens (zone B), the size of the pupillary area at the corneal level (zone C), the area of crossover between zones A and C (zone AC), the area of crossover between zones B and C (BC), the ratio of BC to B (BC/B), and the ratio of AC to C (AC/C). CS was evaluated using the CSV-1000 with spatial frequencies of 3, 6, 12, and 18 cycles/degree (CPD). RESULTS: Multiple correlation analyses indicated significant negative correlations between CS, zone C, BC/B, and 3-mm SIRI (all P<0.01). There were no significant differences between CS, zone B, AC/A, or 5-mm SIRI (P=0.60, 0.94 and 0.11, respectively). Zone C was negatively correlated with 3, 6, 12, and 18 CPD. 5-mm SIRI were negatively correlated with 6, 12, and 18 CPD. BC/C was negatively correlated with 6 and 18 CPD. AC/C was positively correlated with 3 CPD. CONCLUSION: Zone C, 3-mm SIRI and BC/B affect the CS following overnight OK.

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the promoter of MORF4L1 was identified to be significantly higher in tumour cells than in normal cells. The ectopic expression of MORF4L1 was also revealed to inhibit cell proliferation, colony formation, migration and invasion in NPC, whereas the knockdown of MORF4L1 promoted cell proliferation, colony formation, migration and invasion. Mechanistically, the present study demonstrated that MORF4L1 functions as a tumour suppressor by increasing p21 and E-cadherin levels. These findings may be useful novel targets for treating patients with NPC.

LncRNA SNHG5 promotes the progression of osteosarcoma by sponging the miR-212-3p/SGK3 axis.

BACKGROUND: Long non-coding RNA (lncRNA) SNHG5 has been found to play an important role in tumors. Nevertheless, the function and mechanism of lncRNA SNHG5 in osteosarcoma (OS) remains unclear. The purpose of this study was to investigate whether lncRNA SNHG5 can regulate the occurrence and development of OS cells. METHODS: We performed quantitative real time PCR to detect the expression of lncRNA SNHG5 in OS cells. 143B, MG63 (knockdown) and U2OS, U2R (overexpression) cell lines were chosen for the function study of SNHG5. The effect of SNHG5, miR-212-3p, and SGK3 in OS cells was explored by MTT assays, clony formation, flow cytometry, transwell assays, wound healing assays, and cell spreading assays. Quantitative real-time PCR, Western blot analysis and luciferase assays were used to detect the interaction between lncRNA SNHG5 and miR-212-3p. RESULTS: In this study, knockdown of lncRNA SNHG5 suppressed the growth and metastasis of OS cells, whereas the overexpression of SNHG5 produced an opposite result. Mechanistically, lncRNA SNHG5 functions as a sponger against miR-212-3p and suppresses the miR-212-3p/SGK3 signaling pathway. Introduction of miR-212-3p mimics or inhibitors reverses SNHG5 overexpression or silences the exerted tumor promoting or suppressing effect. In addition, our results showed that the function of SNHG5 can be rescued by miR-212-3p and can regulate the growth and metastasis of OS cells via SGK3, the downstream target of miR-212-3p. CONCLUSIONS: In summary, our study demonstrated that lncRNA SNHG5 can regulate the proliferation and metastasis of OS cells through the miR-212-3p/SGK3 axis. This axis may provide a new target for future clinical treatment.

Change in foveal position based on age and axial length in high myopic eyes.

AIM: To evaluate the influence of age and axial length (AL) on the position of the fovea in patients with high myopia (HM). METHODS: In this prospective study, 96 patients (186 eyes) with HM were consecutively recruited from the Third Affiliated Hospital of Nanchang University. DRI-OCT Atlantis, fundus imaging, and IOL Master were used in this study. Three indices were measured: the distance between the fovea and the optic nerve head (ONH) center (DFO), the vertical distance between the fovea and the horizontal line pass of the ONH center (VDFO), and the horizontal distance between the fovea and the vertical line pass of the ONH center (HDFO). These measurements were used to analyze the effects of different age groups (A1, A2, A3 groups) and AL (AL1, AL2, AL3, AL4 groups) on these indices. RESULTS: The results showed that there was no statistical significance in DFO among the age and AL groups (F=0.46, 0.37; P=0.62, 0.76, respectively). In HDFO, there was also no statistical significance among the age and AL groups (F=0.10, 0.48; P=0.90, 0.69, respectively). In VDFO, however, the difference in the age and AL groups was statistically significant (F=3.21, 3.12; P=0.04, 0.02, respectively). Thus, VDFO were correlated with age and AL (r=0.21, 0.23, all P<0.01), while HDFO and DFO were not correlated with age and AL (r=0.30, P>0.05). CONCLUSION: In high myopia, the foveal position changes mainly in the vertical direction along with factors of age and AL.

The decade of exosomal long RNA species: an emerging cancer antagonist.

Exosomes have emerged as a novel approach for the treatment and diagnosis of cancer after RNA content was discovered in exosomes in 2007. As important meditators of intercellular communication, exosomes have become a strong focus of investigation for researchers in the past decade, as witnessed through the exponential increase of research on exosomes. The capability of exosomes to transfer functionally active cargo highlights their importance as promising biomarkers and diagnostic molecules, as well as prospective drug delivery systems. The accessibility of exosomes in nearly all biofluids additionally alludes to its unprecedented ability in various types of cancers due to its extensive impact on tumor formation and progression. This review analyzes the role of exosomal long RNA species, which is comprised of mRNA, lncRNA, and circRNA, in tumor formation and progression, with an emphasis on their potential as future diagnostic biomarkers and treatment vectors in cancer biology. Their alignment with the development of exosomal databases is further examined in this review, in view of the accumulation of studies published on exosomes in the past decade.

NRP1 promotes cell migration and invasion and serves as a therapeutic target in nasopharyngeal carcinoma.

Neuropilin 1 (NRP1) promotes tumor growth, angiogenesis, tumor migration, and invasion. Its higher expression is closely related to the metastasis and poor outcome of many cancers. We have reported that NRP1 was expressed at higher levels in highly metastatic cells in comparison to minimally metastatic cells in nasopharyngeal carcinoma (NPC). However, the role of NRP1 in NPC cell migration and invasion is still unclear, and whether it could serve as a potential therapeutic target for patients with NPC still needs further investigation. In this study, our results demonstrated that ectopic expression of NRP1 in S26 and 6-10B cells promoted cell migration and invasion via wound healing and transwell assays. In contrast, knockdown of NRP1 in HONE1, CNE1 and S18 cells through Clustered Regularly Interspaced Short Palindromic Repeats interference (CRISPRi) technology suppressed cell migration and invasion. Moreover, we found that EG00229, a small molecule inhibitor of NRP1, significantly suppressed NRP1-mediated promotion of NPC cells migration and invasion. Mechanistically, we demonstrated that NRP1 promoted migration and invasion by decreasing E-cadherin levels and increasing N-cadherin levels. Collectively, our results showed that NRP1 promotes cell migration and invasion and could function as a promising target for the future treatment of patients with NPC.