The repeatability and reproducibility of AL-Scan was excellent for all parameters, except WTW and PD. Excluding WTW, good agreement was found between the AL-Scan and IOLMaster. The 2.4-mm diameter K value may be the most reliable choice for calculation of IOL power with the AL-Scan.

No abstract

Ferroptosis, a novel form of regulated cell death, is caused by accumulation of lipid peroxides and excessive iron deposition. This process has been linked to the death of dopaminergic neurons in substantia nigra compacta (SNc) of Parkinson’s disease (PD) patients. Quercetin (QCT), a natural flavonoid, has multiple pharmacological activities. However, it has not been established whether QCT can protect against dopaminergic neuron death by inhibiting ferroptosis. In this study, we investigated the potential antiferroptotic effects of QCT in cellular models established using specific ferroptosis inducers (Erastin and RSL-3) and MPP+. The effects were also explored using MPTP-induced PD mouse models. The cell counting kit-8 (CCK-8) assay was performed to assess cell viability. Variations in mitochondrial morphology were evaluated by transmission electron microscopy (TEM) while the mitochondrial membrane potential, mass, and ROS were measured by fluorescent probes. Lipid peroxidation levels were assayed through measurement of lipid ROS, MDA, GSH, and SOD levels. The effects of QCT on MPTP-induced behavioral disorders were examined by rotarod and open field tests. In vitro and in vivo, QCT significantly inhibited ferroptosis by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) protein. Additionally, QCT ameliorated motor behavioral impairments and protected against the loss of dopaminergic neurons in MPTP-induced PD models. Interestingly, Nrf2 knockdown alleviated the protective effects of QCT against ferroptosis. In conclusion, these results demonstrate that ferroptosis is involved in MPP+/MPTP-induced PD, and QCT inhibits ferroptosis by activating the Nrf2 protein. Therefore, QCT is a potential agent for preventing the loss of dopaminergic neurons by targeting ferroptosis.

Rock fragment cover has long been an important agricultural crop production technique on the Loess Plateau, China. Although this approach plays an important role in controlling hydrological processes and preventing soil erosion, inconsistent results have been recovered in this field. In this study, we investigated the effects of rock fragment cover on infiltration, run‐off, soil erosion, and hydraulic parameters using rainfall simulation in the field in a semi‐arid region of China. Two field plots encompassing 6 rock fragment coverages (0%, 10%, 20%, 25%, 30%, and 40%), as well as 2 rock fragment positions and sizes were exposed to rainfall at a particular intensity (60 mm h−1). The results of this study showed that increasing the rock fragment coverage with rock fragments resting on the soil surface increased infiltration but decreased run‐off generation and sediment yield. A contrasting result was found, however, when rock fragments were partially embedded into the soil surface; in this case, a positive relationship between rock fragment coverage and run‐off rate as well as a nonmonotonic relationship with respect to soil loss rate was recovered. The size of rock fragments also exerted a positive effect on run‐off generation and sediment yield but had a negative effect on infiltration. At the same time, both mean flow velocity and Froude number decreased with increasing rock fragment coverage regardless of rock fragment position and size, whereas both Manning roughness and Darcy–Weisbach friction factor were positively correlated. Results show that stream power is the most sensitive hydraulic parameter affecting soil loss. Combined with variance analysis, we concluded that the order of significance of rock fragment cover variables was position followed by coverage and then size. We also quantitatively incorporated the effects of rock fragment cover on soil loss via the C and K factors in the Revised Universal Soil Loss Equation. Overall, this study will enable the development of more accurate modelling approaches and lead to a better understanding of hydrological processes under rock fragment cover conditions.

Background: Emerging evidence indicates that the apolipoprotein E (APOE) ε4 exacerbates α-synuclein pathology. Objective: To determine whether APOE ε4 contributes to motor progression in early Parkinson's disease (PD). Methods: Longitudinal data were obtained from 384 patients with PD divided into APOE ε4 carriers (n = 85) and noncarriers (n = 299) in the Parkinson's Progression Marker Initiative. Participants underwent yearly motor assessments over a mean follow-up period of 78.9 months. Repeated measures and linear mixed models were used to test the effects of APOE ε4. Results: The motor progression was significantly more rapid in patients with PD carrying APOE ε4 than in noncarriers (β = 0.283, P = 0.026, 95% confidence interval: 0.033-0.532). Through subgroup analysis, we found that the effect of APOE ε4 was significant only in patients with high amyloid β burden (β = 0.761, P < 0.001, 95% confidence interval: 0.0356-1.167). Conclusions: APOE ε4 may be associated with rapid motor progression in PD.

Idiopathic pulmonary fibrosis is a progressive interstitial pneumonia characterised by fibroblast accumulation, collagen deposition and extracellular matrix (ECM) remodelling. It was reported that Akt1 mediated idiopathic pulmonary fibrosis progression through regulating the apoptosis of alveolar macrophage, while its effect on macrophage-produced cytokines remains largely unknown. In the present study, we first examined the phosphorylation of Akt1 in lung sections from idiopathic pulmonary fibrosis patients by immunohistochemistry before applying a bleomycin-induced idiopathic pulmonary fibrosis model using Akt1−/− mice and Akt1+/+ littermates. The results showed that Akt1 was remarkably up-regulated in idiopathic pulmonary fibrosis patients, while in vivo studies revealed that Akt1-deficient mice had well-preserved alveolar structure and fewer collagens, secreted fewer matrix components, including alpha smooth-muscle actin and fibronectin and survived significantly longer than Akt1+/+ littermates. Additionally, the pro-fibrogenic cytokine IL-13 was down-regulated at least twofold in Akt1−/−mice compared to the Akt1+/+group on d 3 and 7 after bleomycin treatment. Furthermore, it was found that Akt1–/– macrophages displayed down-regulation of IL-13 compared to Akt1+/+ macrophages in which Akt1 was phosphorylated in response to IL-33 stimulation. These findings indicate that Akt1 modulates pulmonary fibrosis through inducing IL-13 production by macrophages, suggesting that targeting Akt1 may simultaneously block the fibrogenic processes of idiopathic pulmonary fibrosis.

No abstract

No abstract