A comparative study of ultrasound cycloplasty and endoscopic cyclophotocoagulation in the treatment of secondary glaucoma.

To compare the clinical efficacy of ultrasound cycloplasty (UCP) and endoscopic cyclophotocoagulation (ECP) in the treatment of secondary glaucoma. In a 12-month prospective single-center study, 22 patients with secondary glaucoma were treated by high-intensity focused ultrasound (HIFU), and 23 patients with secondary glaucoma were treated by a semiconductor laser. At the final follow-up, the two groups' surgical outcomes were compared. A complete success was defined as an intraocular pressure (IOP) reduction of at least 20% from baseline and an IOP of > 5 mmHg and ≦ 21 mmHg, while a qualified success was defined as an IOP reduction of at least 20% from baseline and an IOP of > 5 mmHg. The secondary outcome was the average IOP, number of drugs, and complications at each follow-up compared with the baseline. The average preoperative IOPs in the UCP and ECP groups were 36.4 ± 9.5 mmHg (n = 2.3 drops, n = 0.2 tablets) and 34.5 ± 11.7 mmHg (n = 2.0 drops, n = 0.3 tablets), respectively. In the last follow-up, the success rate of UCP was 54% (with a decrease of 32%) and that of ECP was 65% (with a decrease of 35%), and the P-value between the two groups was > 0.05. However, there was a difference in the average IOP between these two groups 1 day and 1 week after the operation, and the IOP reduction efficiency in the ECP group was better. However, the amount of drug used after these two surgeries was significantly reduced. There were fewer postoperative complications in the UCP group (18 cases) than in the ECP group (35 cases). Both UCP and ECP can effectively reduce IOP in secondary glaucoma, and ECP has a better effect at the early stages. However, UCP has higher safety and tolerance for patients.

FSTL3 Induces Lipid Accumulation and Inflammatory Response in Macrophages and Associates With Atherosclerosis.

FSTL3 as adipokine takes part in dyslipidemia and inflammatory response, but the association of FSTL3 with atherosclerosis is unclear. This study indicated that FSTL3 showed significantly higher level (control: 7.68 ± 3.10 vs. AS: 9.29 ± 2.37 ng/mL; P < 0.001) in atherosclerosis, and FSTL3 expressed higher in plaque of ApoE knockout mice and located in macrophages. Oxidized low-density lipoproteins induced expression and secretion of FSTL3, meanwhile FSTL3 promoted lipid accumulation in macrophages. The advanced study found that FSTL3 upregulated CD36 and LOX-1 expression in a dose-dependent manner; however, FSTL3 also evoked interleukin 1-ß (IL1-ß), monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor-α, and matrix metalloproteinase-9 (MMP-9) secretion in macrophages. On the contrary, that downregulated FSTL3 attenuated expression of oxidized low-density lipoproteins induced CD36, LOX-1, and inflammatory cytokines expressing. All of these results demonstrated that FSTL3 as a novelty cytokine takes part in the process of atherosclerosis through increasing lipid accumulation and inflammation through regulating CD36 and LOX-1 expression.

Heavy smoking before coronary surgical procedures affects the native matrix metalloproteinase-2 and matrix metalloproteinase-9 gene expression in saphenous vein conduits.

BACKGROUND: Smoking has numerous effects that may promote atherosclerosis, but the pathogenesis of smoking-related vein graft disease after coronary artery bypass grafting (CABG) remains incompletely understood. Matrix metalloproteinase (MMP) subtypes MMP-2 and MMP-9 have been identified as the key components in vascular remodeling processes. However little is known about the native MMP2 and MMP9 gene expression in saphenous vein (SV) conduits of heavy smokers undergoing CABG. METHODS: Two hundred eight patients were divided into 6 groups: nonsmokers, heavy smokers, 3-month quitters, 6-month quitters, 12-month quitters, and long-term quitters. mRNA and protein levels of MMP-2, MMP-9, and tissue inhibitors of metalloproteinases (TIMPs) 1 and TIMP-2 were analyzed. In a clinical study, SV graft patency after surgical procedures was followed up. RESULTS: Compared with the nonsmoker group, MMP2 and MMP9 gene expression was significantly increased in the other 5 groups (p < 0.05). In contrast to MMP response, TIMP1 and TIMP2 gene expression was significantly decreased (p < 0.05). An association of increased MMP2 and MMP9 gene expression with poor SV graft patency could be found in the clinical data from follow-up. CONCLUSIONS: Heavy smoking noticeably increases native MMP2 and MMP9 gene expression in the SV before CABG. Even after long-term cessation of smoking, the dysregulated MMP2 and MMP9 gene expression cannot recover to normal levels. With the elevated native MMP2 and MMP9 gene expression in the SV induced by heavy smoking, more vein graft disease can be found on long-term follow-up.

Oxidative stress induced by urban fine particles in cultured EA.hy926 cells.

It has been reported that vascular endothelia cell damage is an important precursor to the morbidity and mortality associated with cardiovascular disease exposed to airborne particulate matter (PM). The present study investigated the hypothesis that urban fine (PM(2.5)) particles could cause cytotoxicity via oxidative stress in human umbilical vein endothelial cells, EA.hy926. The concentrations of metal elements (Cr, Fe, Ni, Cu, Zn, Mo, Cd and Pb) in PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) were determined by inductively coupled plasma - mass spectrometry (ICP-MS). Iron (Fe), Zn and Pb were highly enriched in all the samples. Exposure of the cultured EA.hy926 cells to PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) led to cell death, reactive oxygen species (ROS) increase, mitochondrial transmembrane potential (ΔΨm) disruption and NF-κB activation, respectively. The ROS increase by exposure to PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) triggered the activation of nuclear factor (NF)-κB, which means that PM(2.5) particles exert cytotoxicity by an apopotic process. However, the induction of cytotoxicity by PM(2.5) suspension, water-soluble and water-insoluble fractions of PM(2.5) was reversed by pretreatment with superoxide dismutase (SOD). These results suggest that each fraction of PM(2.5) has a potency to cause oxidative stress in endothelial cells. ROS was generated through PM(2.5)-mediated mitochondrial apoptotic pathway, which may induce direct interaction between metal elements and endothelia cells.