Disorder of blood-aqueous barrier following Ahmed Glaucoma Valve implantation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Ahmed Glaucoma Valve implantation (AGVI) is used to treat refractory glaucoma. Breakdown of the blood-aqueous barrier (BAB) has been noted after some surgical techniques. The current study was designed to assess BAB disruption after AGVI.</p><p><b>METHODS</b>Anterior chamber protein content was measured by the laser flare cell photometry in 22 eyes of 22 patients with refractory glaucoma before AGVI and at each postoperative visit up to 1 month.</p><p><b>RESULTS</b>Before AGVI the mean aqueous flare values in all eyes were (15.17 ± 9.84) photon counts/ms. After AGVI, the values significantly increased at day 1, day 3, and week 1 compared to those before AGVI (all P < 0.05) with a peak at day 3. They returned to pre-operative levels at week 2, and were lower than preoperative level at month 1. Eyes with previous intraocular surgery history had greater aqueous flare values than those without previous intraocular surgery history, but there were no significant differences at all time points postoperatively (all P > 0.05). Furthermore, eyes with shallow anterior chambers had greater aqueous flare values at day 3 and week 1 (all P < 0.05). When comparing eyes with other refractory glaucoma conditions, neovascular glaucoma combined with intravitreal bevacizumab injection resulted in lower aqueous flare values after AGVI, but no significant differences were observed at all time points, postoperatively (all P > 0.05).</p><p><b>CONCLUSIONS</b>The BAB was impaired and inflammation was present in the anterior chamber in refractory glaucomatous eyes following AGVI. However, such conditions were resolved within 1 month postoperatively. Intravitreal bevacizumab treatment in neovascular glaucoma eyes before AGVI may prevent BAB breakdown.</p>

Adjunctive with versus without intravitreal bevacizumab injection before Ahmed glaucoma valve implantation in the treatment of neovascular glaucoma / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Neovascular glaucoma (NVG) is a refractory disease which is difficult to manage. This study aimed at evaluating the efficacy and safety of adjunctive intravitreal bevacizumab (IVB) injection in conjunction with Ahmed glaucoma valve implantation (AGVI) in the management of NVG.</p><p><b>METHODS</b>This was a retrospective study of patients with NVG in whom AGVI was performed between October 2008 and May 2012. The sample was divided into two groups according to the pretreatment: with adjunctive IVB injection (the IVB group, n = 25 eyes) and without adjunctive IVB injection (the control group, n = 28 eyes). The surgical success rate, number of antiglaucoma medications used, best-corrected visual acuity (BCVA), postoperative complications, regression, and recurrence of iris neovascularization (NVI) were analyzed between the groups.</p><p><b>RESULTS</b>The surgical outcomes of the two groups were compared. The complete success rates in the IVB and control groups were 84.0% and 64.3% at 12 months and 80.0% and 53.6% at 18 months, respectively. There was a significant difference between the two groups (P = 0.041). Mean postoperative intraocular pressures, mean number of postoperative antiglaucoma medications, and BCVA were not significant between the two groups. The NVI in 22 (88.0%) eyes had completely regressed within 2 - 8 days after IVB. However, NVI recurred in 10 eyes (40.0%) 2 - 9 months later after IVB. The IVB group had only 1 case (4.0%) of hyphema out of 25 eyes, while there were 8 (28.6%) cases of hyphema out of 28 eyes in the control group (P = 0.026).</p><p><b>CONCLUSIONS</b>This study showed that preoperative IVB injection reduced NVI remarkably, decreased hyphema, and led to higher surgical success rates. Pre-operative IVB injection may be an effective adjunct to AGVI in the management of NVG.</p>

Neuroprotection in glaucoma: present and future / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To review the updated research on neuroprotection in glaucoma, and summarize the potential agents investigated so far.</p><p><b>DATA SOURCES</b>The data in this review were collected from PubMed and Google Scholar databases published in English up to September 2012, with keywords including glaucoma, neuroprotection, and retinal ganglion cells, both alone and in combination. Publications from the past ten years were selected, but important older articles were not excluded.</p><p><b>STUDY SELECTION</b>Articles about neuroprotection in glaucoma were selected and reviewed, and those that are cited in articles identified by this search strategy and judged relevant to this review were also included.</p><p><b>RESULTS</b>Although lowering the intraocular pressure is the only therapy approved as being effective in the treatment of glaucoma, increasing numbers of studies have discovered various mechanisms of retinal ganglion cells death in the glaucoma and relevant neuroprotective strategies. These strategies target neurotrophic factor deprivation, excitotoxic damage, oxidative stress, mitochondrial dysfunction, inflammation, activation of intrinsic and extrinsic apoptotic signals, ischemia, and protein misfolding. Exploring the mechanism of axonal transport failure, synaptic dysfunction, the glial system in glaucoma, and stem cell used in glaucoma constitute promising research areas of the future.</p><p><b>CONCLUSIONS</b>Neuroprotective strategies continue to be refined, and future deep investment in researching the pathogenesis of glaucoma may provide novel and practical neuroprotection tactics. Establishing a system to assess the effects of neuroprotection treatments may further facilitate this research.</p>

Role of PI3K/Akt signaling in the protective effect of magnesium sulfate against ischemia-perfusion injury of small intestine in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The protective effects of magnesium sulfate against ischemia-reperfusion injury of the small intestine in Sprague-Dawley (SD) rats have been confirmed in our previous research. However, its exact mechanism is unclear. This study was to evaluate the role of PI3K/Akt signal pathway in the protective effect of magnesium sulfate against ischemia-reperfusion injury of the small intestine in SD rats.</p><p><b>METHODS</b>Rat model of intestinal ischemia-reperfusion injury was used. The SD rats were divided into four groups randomly: sham operation group, ischemia-reperfusion group, magnesium sulfate group and magnesium sulfate plus LY294002 (an inhibitor of PI3K) group. The pathological changes of intestinal mucosa were examined; the activity of diamine oxidase (DAO) in plasma, the plasma contents of malondialdehyde (MDA), and apoptosis rate of the intestinal mucosal cells were determined and compared. The expression of p-Akt was detected by Western blotting.</p><p><b>RESULTS</b>There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), enhanced DAO activity (P < 0.05), elevated contents of MDA (P < 0.05), higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the ischemia-reperfusion group compared with the sham operation group. There were less evident pathological changes of the intestinal mucosa (lower Chiu's score, P < 0.05), lower DAO activity (P < 0.05), lower contents of MDA (P < 0.05), and lower apoptosis rate (P < 0.05), but higher level of p-Akt (P < 0.05) in the magnesium sulfate group compared with the ischemia-reperfusion group. There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), higher contents of MDA (P < 0.05), higher DAO activity (P < 0.05) and higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the magnesium sulfate plus LY294002 group compared with the magnesium sulfate group.</p><p><b>CONCLUSIONS</b>Activation of PI3K/Akt signal pathway results in the reduction of cell apoptosis, which likely accounts for the protective effect of magnesium sulfate against intestinal ischemia-reperfusion injury.</p>