ABSTRACT
Objective To evaluate the surgically induced astigmatism (SIA)caused by coaxial phacoemuisification and intraocular lens (IOL) implantation with different clear corneal incision.Methods Clinical data of 97 patients 97 eyes underwent phacoemulsification and IOL implantation with 2.2 mm (2.2 mm group,44 eyes) or 2.8mm (2.8 mm group,53 eyes) clear corneal incisions were retrospectively reviewed.The corneal curvature were measured before and four weeks after the surgery.Then SIA were calculated,followed by analysis of the differences in mean SIA and centroid SIA between the 2.2 mm and 2.8 mm groups.Results At 4 weeks after surgery,the centroid and mean SIA of the 2.8 mm group was (0.234 ± 0.423) D@105° and (0.552 ±0.349) D,respectively;the corresponding data was (0.174 ± 0.464) D@104° and (0.582 ±0.392) D in the right eyes,and (0.272 ±0.382)D@106° and (0.545 ±0.300) D in the left eyes,respectively.At 4 weeks after surgery,the centroid and mean SIA of the 2.2 mm group was (0.108 ±0.417)D@98°and (0.506 ±0.362) D,respectively;the corresponding data was (0.145 ±0.404)D@81° and (0.5182 ±0.332)D in the right eyes,and (0.127 ± 0.418) D@120° and (0.516 ± 0.418) D in the left eyes,respectively.There was no significant difference in centroid SIA and mean SIA,centroid SIA and mean SIA of the right and left eyes,as well as both eyes between the two groups (all P＞0.05);Atotal of 47 patients (48.5％) had SIA greater than 0.5 D,and 28 patients (52.8％) were in the 2.8 mm groups,including 12 patients (22.6％) in the right eyes and 16 patients (20.5％) in the left eyes;as well as 19 patients (43.2％) in the 2.2 mm group,including 10 patients (22.7％) in the right eyes and 9 patients (20.5％) in the left eyes.There was no significant difference in the proportion of SIA greater than 0.5 D and the proportion of SIA between the left and right eyes greater than 0.5 D between the two groups (all P ＞ 0.05).Conclusion The mean SIA and centroid SIA are not statistically different in the 2.2 mm group than in the 2.8 mm group,but SIA were more stable in the 2.2 mm group than in the 2.8 mm group.The axis of the SIA were closely related to the position of the incisions,which were the vertical direction of the incisions.
ABSTRACT
β-Glucan is a kind of highly conservative composition on fungal cell wall.As a recognition receptor of β-glucan,dendriticcell-associatedC-typelectin-1 (dectin-1)widely distributeinsingle-nuclea macrophages system,dendritic cells ( DC )and neutrophil cells.Through the identification of fungal cell wall composition and cells signal transduction,dectin-1 induces the production of cytokine and chemokine and then starts a nonspecific and specific immunity response.Dectin-1 plays a key role in antifungal immune response.Here,the molecular structure,tissue cells,signal transmission and the immune inflammation role of dectin-1 in corneal infection were reviewed.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the influence of endothelial dysfunction induced by inoculated dendritic cells (DCs) loaded heat shock protein 60 (HSP60) in apolipoprotein (Apo) E-null mice, and the effect of Puerarin on it.</p><p><b>METHODS</b>HSP60 DC (DChsp) acquired after prepared bone marrow-derived DCs of ApoE-null mice and treated with HSP60. In vitro, the function of DCs and the effect of Puerarin were detected. While in vivo, ApoE-null mice fed with high-cholesterol forage were divided into two groups and intravenous inoculated with DCh-sp or normal saline via vein twice respectively. The mice in the two groups were subdivided into the Puerarin group and non-treated group, and they were injected intraperitoneally with Puerarin and normal saline at the beginning of inoculation and the following 3 weeks, respectively. In addition, C57BL/6 mice without inoculation were taken as the normal control group. Two weeks after the last time inoculated, the response of T lymphocytes to HSP60 and endothelial-dependent diastolic function of aortic ring were detected.</p><p><b>RESULTS</b>HSP60 could promote DCs expressed CD86 and stimulate T lymphocytes proliferation in vitro, while Puerarin had significantly inhibitory effect. After inoculated, DChsp activated inflammatory response in vivo and aggravated endothelium-dependent dilation in mice. Puerarin could significantly inhibit inflammatory reaction caused by DChsp and improve endothelium dilation.</p><p><b>CONCLUSION</b>Hsp60 could activate DCs in vitro and in vivo, Puerarin could significantly inhibit specific immunity induced by HSP60 and improve vascular endothelium-dependent dilation.</p>