FS-LASIK demonstrated a greater increase in PCE than SMILE only at 12 months, as well as a greater reduction of CRF than SMILE. There were no significant differences in PCE change over time within either group.

Epidemiological surveys indicate that the incidence of inflammatory bowel disease (IBD) is increasing rapidly with the continuous growth of the economy. A large number of studies have investigated the relationship between the genetic factors related to the susceptibility to IBD and the gut microbiota of patients by using high-throughput sequencing. IBD is considered the outcome of the interaction between host and microorganisms, including intestinal microbial factors, abnormal immune response, and a damaged intestinal mucosal barrier. The imbalance of microbial homeostasis leads to the colonization and invasion of opportunistic pathogens in the gut, which increases the risk of the host immune response and promotes the development of IBD. It is critical to identify the specific pathogens related to the pathogenesis of IBD. An in-depth understanding of various pathogenic factors is of great significance for the early detection of IBD. This review highlights the role of gut microbiota in the pathogenesis of IBD and provides a theoretical basis for the personalized approaches that modulate the gut microbiota to treat IBD.

In the present study, we examined the mechanisms of oxaliplatin-induced drug resistance in human colorectal cancer cell lines HT29 and HCT116. Our results demonstrate a significant autophagy expression in CRC cells after an oxaliplatin treatment. Administration of oxaliplatin to human CRC cells significantly enhanced the expression of HMGB1, which regulated the autophagy response and negatively regulate the cell apoptosis. Moreover, a decreased oxaliplatin -induced autophagy response and an increased apoptosis level were detected in stable CRC cells harboring HMGB1 shRNA. Then we noted that HMGB1 significantly induced extracellular signal-regulated kinase (ERK)/Extracellular signal-regulated kinase kinase (MEK) phosphorylation. Taken together, these data suggest that HMGB1-mediated autophagy modulates sensitivity of colorectal cancer cells to oxaliplatin via MEK/ERK signaling pathway.

PURPOSE. To conduct in vivo measurements of the bulbar conjunctiva epithelial, stromal, and total thicknesses in healthy Chinese subjects using optical coherence tomography (OCT) and to compare the conjunctival thickness differences between sex and age.METHODS. From January to July 2012, healthy Chinese subjects were recruited to undergo a Cirrus HD-OCT examination using the Anterior Segment 5 Line Raster scanning protocol. Ophthalmoscopy and slit-lamp examinations were performed on all eyes, along with the determination of visual acuity. The bulbar conjunctiva epithelial thickness, stromal thickness, and full thickness were measured on cross-sectional conjunctiva images. The average values of each parameter were compared between males and females and among eight age groups (<20, 21-30, 31-40, 41-50, 51-60, 61-70, 71-80, and >80 years). RESULTS.A total of 711 eyes in 711 subjects (average age 46.5 years) were included. The average conjunctiva epithelial, stromal, and full thickness measurements were 42.4 6 7.4 lm, 197.7 6 32.5 lm, and 240.1 6 29.8 lm, respectively. No significant difference was found for any of the three parameters between sexes. The conjunctiva epithelial thickness values decreased significantly after age 20 and were then maintained at relatively low levels, followed by a sharp increase at 60 years of age. The conjunctiva stromal thickness decreased throughout the entire lifetime, and the full thickness decreased from the teenage to the elderly periods.CONCLUSIONS. None of the Chinese conjunctiva epithelial, stromal, and full thickness was sexrelated, but all of them were age-related.

Recent studies have considered thwarting false data injection (FDI) attacks against state estimation in power grids by proactively perturbing branch susceptances. This approach is known as moving target defense (MTD). However, despite of the deployment of MTD, it is still possible for the attacker to launch stealthy FDI attacks generated with former branch susceptances. In this paper, we prove that, an MTD has the capability to thwart all FDI attacks constructed with former branch susceptances only if (i) the number of branches l in the power system is not less than twice that of the system states n (i.e., l ≥ 2n, where n + 1 is the number of buses); (ii) the susceptances of more than n branches, which cover all buses, are perturbed. Moreover, we prove that the state variable of a bus that is only connected by a single branch (no matter it is perturbed or not) can always be modified by the attacker. Nevertheless, in order to reduce the attack opportunities of potential attackers, we first exploit the impact of the susceptance perturbation magnitude on the dimension of the stealthy attack space, in which the attack vector is constructed with former branch susceptances. Then, we propose that, by perturbing an appropriate set of branches, we can minimize the dimension of the stealthy attack space and maximize the number of covered buses. Besides, we consider the increasing operation cost caused by the activation of MTD. Finally, we conduct extensive simulations to illustrate our findings with IEEE standard test power systems.