Currently, exosomes rich in RNAs and proteins are regarded as vital mediators of intercellular communication. Here, we aimed to explore the effects of exosomal miR-1290 in gastric cancer (GC) and understand its mechanism of action on GC progression. We first isolated exosomes from serum samples of GC patients and healthy people and characterized them by transmission electron microscopy. Then, we examined the expression level of miR-1290 contained in the exosomes by quantitative reverse-transcription polymerase chain reaction and found that exosomal miR-1290 was overexpressed in GC patients and cell lines. Promotion of proliferation, migration, and invasiveness of GC cells was noted after they were incubated with the isolated miR-1290-rich exosomes compared with incubation with a negative control. Furthermore, we predicted that naked cuticle homolog 1 (NKD1) mRNA is a direct target of miR-1290 and confirmed their interaction by a dual luciferase reporter assay. NKD1 overexpression attenuated the stimulatory effects of miR-1290 on GC cells. Collectively, our results suggest that exosomal miR-1290 enhances GC cell proliferation and invasion by targeting NKD1 mRNA and downregulating NKD1 expression. A better understanding of this process may facilitate the development of novel therapeutic agents for GC.

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The cascaded asymmetric exposure long-period fiber gratings are fabricated by CO(2) laser, which provide multi-wavelength filters with anisotropic transmission spectrum under different states of polarization. Inserting this device in the ring cavity of an erbium-doped fiber laser, a triple-wavelength switchable lasing laser with equal spacing of 2.6 nm has been obtained. Owing to the polarization dependent loss of the new cascaded long-period fiber grating, the wavelength switching of random combination of C(1) (3), C (2) (3), and C(3) (3) is demonstrated through the polarization controlling. We derive the wavelength switch to the polarization characteristic of cascaded asymmetric exposure long-period fiber gratings.

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Uncorrected refractive errors are a leading cause of visual impairment across the world. In today's society, laser in situ keratomileusis (LASIK) has become the most commonly performed surgical procedure to correct refractive errors. However, regression of the initially achieved refractive correction has been a widely observed phenomenon following LASIK since its inception more than two decades ago. Despite technological advances in laser refractive surgery and various proposed management strategies, post-LASIK regression is still frequently observed and has significant implications for the long-term visual performance and quality of life of patients. This review explores the mechanism of refractive regression after both myopic and hyperopic LASIK, predisposing risk factors and its clinical course. In addition, current preventative strategies and therapies are also reviewed.

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The osteoblast-derived paracrine factor osteoprotegerin (OPG) is considered to play a key role in inhibition of osteoclast formation and activity. Recently, raloxifene, a nonsteroidal benzothiophene, was found to exert anti-resorptive effects via modulating OPG expression in osteoblasts. To explore whether raloxifene regulates bone metabolism via an OPG-dependant pathway in vivo, we investigated the effects of raloxifene on bone loss in Opg-deficient mice. The results show that bone mineral density and bone strength are increased in mice deficient for Opg after treatment with raloxifene for 30 days. Histomorphometric analysis shows that raloxifene can increase bone trabecular area and decrease the number of osteoclasts in Opg (-/-) mice. Moreover, raloxifene reduces Rankl transcription and serum level of Rankl, which is dramatically increased in Opg knockout mice. These results suggest that raloxifene-induced inhibition of bone resorption may be independent of Opg pathway in mice.

It is well recognized that randomized controlled trials (RCTs) are a powerful tool to investigate causal relationships, and are considered the gold standard level of research evidence. However, RCTs can be expensive and time‐consuming, and when they employ strict eligibility criteria, it results in an unrepresentative population and limited external validity. Recently, the registry‐based randomized clinical trial (RRCT) has emerged as an alternative trial design. Utilizing registries to underpin such studies, RRCTs can have advantages including rapid recruitment, and enhanced generalizability. In Australia, legislated mandatory reporting of cancer diagnoses means that jurisdictional cancer registries are a rich source of systematically collected patient details, representing sound platforms for comprehensive data capture that can serve as a key tool for further research. We review the roles of cancer registries in Australia, discuss important considerations relevant to the design of RRCTs, and outline the opportunities provided by cancer registries to strengthen cancer research.