Purpose To determine myopia progression in children during the COVID-19 and the related factors associated with myopia. Methods All subjects underwent three-timepoint ocular examinations that were measured in July 2019, January, and August 2020. We compared the changes in uncorrected visual acuity (UCVA), mydriatic spherical equivalent (SE), and axial length (AL) between two periods (before and during COVID-19). A questionnaire was performed to investigate risk factors for myopia. Results Compared with before the COVID-19, the mean (S.D.) myopia progression during the COVID-19 was significantly higher in right eyes (− 0.93 (0.65) vs. − 0.33 (0.47) D; p < 0.001). However, the differences in UCVA changes and the axial elongation between two periods were clinically insignificant. Through logistic regressive analysis, we found the difference of the SE changes was associated with the baseline AL (P = 0.028; 95% confidence interval [CI], 1.058, 2.632), online education (P = 0.02; 95% CI, 1.587, 8.665), and time of digital screen (p < 0.005; 95% CI, 1.587, 4.450). Conclusions Children were at higher risk of myopia progression during COVID-19, which was associated with the baseline AL, the longtime online learning, and digital screen reading.

Aims: Macrophage (MΦ) infiltration during myocardial infarction (MI) amplifies cardiac inflammation and remodeling. We investigated whether activation of the NRLP3 inflammasome by a calcium sensing receptor (CaSR) in MΦ subsets contributes to cardiac remodeling following MI. Methods and Results: Infiltrated MΦ exhibited biphasic activation after MI; M1MΦ peaked at MI 3d and decreased until MI 14d, whereas M2MΦ peaked at MI 7d and decreased at MI 14d as shown via immunohistochemistry. IL-1β co-infiltrated with both M1MΦ and M2MΦ; IL-1β exhibited the same infiltrating tendency as M1MΦ, which was detected by immunohistochemistry. Increasing ventricular fibrosis was confirmed by Masson staining. CaSR and NLRP3 inflammasome in the MI group were upregulated in MΦ subsets in myocardium and peritoneal MΦ (p-MΦ) compared with the sham groups which were detected by immunofluorescence and western blotting. CaSR-activated NLRP3 inflammasome played a role in M1MΦ via PLC-IP₃ but did not play a role in M2MΦ which were polarized by the THP-1 as shown by western blotting and intracellular calcium measurement. CaSR/NLRP3 inflammasome activation in M1MΦ led to the following effects: upregulated α-sma, MMP-2 and MMP-9, and collagen secretion; and downregulated TIMP-2 in cardiac fibroblasts via IL-1β-IL-1RI, which was detected by coculturing M1MΦ and cardiac fibroblasts. Conclusions: We suggest that the CaSR/NLRP3 inflammasome plays an essential role via the PLC-IP₃ pathway in M1MΦ to promote cardiac remodeling post-MI in rats, including accelerated cardiac fibroblast phenotypic transversion, increased collagen and extracellular matrix (ECM) secretion; however, the CaSR/NLRP3 inflammasome does not play a role in this process in M2MΦ.

Background: To assess the impact of study-at-home during the COVID-19 pandemic on myopia development in Chinese schoolchildren.Methods: This historical cohort involved two groups with a total of 154 children. The exposed group was formed from 77 children aged 8 to 10 years who studied at home in the 7-month period during the COVID-19 pandemic (follow-up period: January – August 2020) and did not study at home in the 7-month period before the COVID-19 outbreak (baseline period: July 2019 – January 2020). Seventy-seven children who did not undergo study-at-home (baseline period: 7 months in 2015, follow-up period: 7 months in 2016) were included in the control group. Cycloplegic refraction, axial length and uncorrected visual acuity were measured 3 times. The questionnaire mainly focused on collecting visual habits.Results: Myopia progression was similar between the two groups in the baseline period. However, in the follow-up period the exposed group had a greater change in refraction toward myopia (−0.83 ± 0.56 D) than the control group (−0.28 ± 0.54 D; p &lt; 0.001). In addition, the exposed group exhibited a significantly greater change in refraction toward myopia in the follow-up period (−0.83 ± 0.56 D) than in the baseline period (−0.33 ± 0.46 D; p &lt; 0.001). Difference-in-difference analysis indicated that study-at-home accelerated the change in refraction toward myopia (t = −0.567; p &lt; 0.001).Conclusions: During the COVID-19 pandemic study-at-home accelerated the change of refraction toward myopia in children.

Engineered nanoparticles (ENPs) have been widely applied in industry, commodities, biology and medicine recently. The potential for many related threats to human health has been highlighted. ENPs with their sizes no larger than 100 nm are able to enter the human body and accumulate in organs such as brain, liver, lung, testes, etc, and cause toxic effects. Many references have studied ENP effects on the cells of different organs with related cell apoptosis noted. Understanding such pathways towards ENP induced apoptosis may aid in the design of effective cancer targeting ENP drugs. Such ENPs can either have a direct effect towards cancer cell apoptosis or can be used as drug delivery agents. Characteristics of ENPs, such as sizes, shape, forms, charges and surface modifications are all seen to play a role in determining their toxicity in target cells. Specific modifications of such characteristics can be applied to reduce ENP bioactivity and thus alleviate unwanted cytotoxicity, without affecting the intended function. This provides an opportunity to design ENPs with minimum toxicity to non-targeted cells.

The objective of this study was to develop a novel scaffold imitating the ingredients and their ratios of natural dermal matrix and to evaluate its biological activity. We applied different ratios and different synthetic methods to fabricate nine kinds of cross-linked (CL) collagen/chondroitin sulfate/hyaluronic acid (Co/CS/HA) scaffolds for dermal tissue engineering. On the basis of comparison among the morphology, mechanical properties, and biodegradation rates of scaffolds, we selected the novel scaffold that was fabricated under unique procedures. In the procedures, Co, CS, and HA were firstly synthesized together in the ratio of 9:1:1 to form a membrane that was then CL with 5 mM of 1-ethyl-3-3-dimethylaminopropylcarbodiimide hydrochloride (EDC) (Co-CS-HA/CL 9:1:1). From the results of comparison, we also found that the ratio of 9:1:1 was better than other ratios. So the scaffold of Co-CS-HA/CL 9:1:1 was used as experimental group with the scaffolds of Co-HA/CS CL 9:1:1 and Co-CS/HA CL 9:1:1 as control groups to evaluate their characteristics in vitro. A control group of an open wound without scaffold was supplemented to evaluate their effects on promoting wound healing in vivo. Morphological observation showed that the novel Co-CS-HA/CL 9:1:1 scaffold had uniform and widely interconnected pores with mean diameters of 109 +/- 11 microm and adequate porosity of about 94%. Mechanical property and biodegradation assessment indicated that it had more degradation-resistant and higher elastic modulus than other scaffolds. Metabolic activity assay showed that it could more strongly promote cellular attachment and proliferation. When scaffolds were seeded with allogenic skin fibroblasts and implanted on the dorsum of Sprague-Dawley rats for 6 weeks, the novel Co-CS-HA/CL 9:1:1 skin equivalent could more successfully repair full thickness skin defects in Sprague-Dawley rats. The histology was more approximate to normal skin than those of the controls within 6 weeks. These results demonstrated that the novel CoCS-HA/CL 9:1:1 tri-copolymer has the potential to be used as a scaffold for dermal tissue engineering.

Lipopolysaccharide (LPS)-induced oxidative stress is a main feature observed in the sepsis by increasing endothelial oxidative damage. Many studies have demonstrated that Ulinastatin (UTI) can inhibit pro-inflammatory proteases, decrease inflammatory cytokine levels and suppress oxidative stress. However, the potential molecular mechanism underlying UTI which exerts its antioxidant effect is not well understood. In this study, we aimed to investigate the effects of UTI on the LPS-induced oxidative stress and the underlying mechanisms using human umbilical vein endothelial cells (HUVECs). After oxidative stress induced By LPS in HUVECs, the cell viability and reactive oxygen species (ROS) in cytoplasm were measured. In addition, superoxide dismutase (SOD) and malondialdehyde (MDA) were examined. We found that LPS resulted in a profound elevation of ROS production and MDA levels. The decrease in Cu/Zn-SOD protein and increased in Mn-SOD protein were observed in a time- and dose-dependent manner. These responses were suppressed by an addition of UTI. The increase in c-Jun N-terminal kinases (JNK) phosphorylation by LPS in HUVECs was markedly blocked by UTI or JNK inhibitor SP600125. Our results suggest that UTI exerts its anti-oxidant effects by decreasing overproduction of ROS induced by LPS via suppressing JNK/c-Jun phosphorylation. Therefore UTI may play a protective role in vascular endothelial injury induced by oxidative stress such as sepsis. This study may provide insight into a possible molecular mechanism by which Ulinastatin inhibits LPS-induced oxidative stress.

Kinesins are essential for the proper function of many types of polar cells, including epithelial cells, neurons, and sperm. Spermatogenesis is closely associated with many different kinesins. These kinesins participate in several fundamental processes, including mitotic and meiotic division, essential organelle transport, and the biogenesis of peculiar structures for the formation of mature sperm. Kinesin-13, kinesin-8, and the chromokinesin families cooperate to ensure normal sister chromatid congression and segregation. The kinesin-8 family motor KIF18A, kinesin-12 motors PAKRP/kinesin12A and PAKRP1L/kinesin12B, and other kinesin-like motors are essential in the process of homologous chromosome pairing and in the separation to create haploid gametes. During spermiogenesis, the responsibility of a handful of kinesin members lies in the maturation of spermatids into mature, motile, and intact spermatozoa. Such roles are completed upon the release of viable and functional sperm into the lumen of seminiferous tubules. In this process, KIFC1, KIF5C, KRP3A, and KRP3B may be involved in acrosome biogenesis; KIFC1, KIFC5, CHO2, KIF17b, and KIF3A probably contribute to nuclear shaping; KIF17b, KIF3A, and KLC3 are implicated in the tail formation process; and KIF20 and KRP3 likely participate in sperm translocation. KIF17b also exhibited postmeiosis transcriptional activities that are critical for the dramatic alterations observed in nuclear and cytoplasmic structures. This review summarizes the roles of kinesins during mitosis, meiosis, and spermiogenesis, and proposes several important issues for further investigation.

The documents on Metallothioneins (MTs) in aquatic creatures, especially focusing on their function as biomarkers in environmental monitoring programmes, are vast and increasing. There are, however, few papers to summary the physiological role of MTs in aquatic organisms especially on development. The multifaceted roles of MTs include involvement in homeostasis, protection against heavy metals and oxidant damages, and metabolic regulation, sequestration and/or redox control. In this paper, we have collected published information on MTs in aquatic organisms-pisces, amphibians, mammals, etc., and analyzed their function in these aquatic animals. MTs have four main functions in aquatic vertebrate. They are respectively bioaccumulation of toxic metals and detoxification, homeostatic regulation of metals, protection against oxidative stress and neuroprotective mechanism. MTs separate in different tissues and they have various distributions in different tissues of aquatic vertebrate, including liver, gills, kidney, testes, and brain. MTs can be induced by a variety of environmental and physiological factors, among which, heavy metals are the main kind of MTs inducers in aquatic vertebrate. Here we pay more attention on the essential metals copper (Cu) and zinc (Zn) and the non-essential metals cadmium (Cd), silver (Ag), lead (Pb), and mercury (Hg).