Success and complications of endoscopic laser dacryocystorhinostomy vs. external dacryocystorhinostomy: A systematic review and meta-analysis.

A systematic review and meta-analysis were conducted to evaluate the success and complications of endoscopic laser dacryocystorhinostomy (ELDCR) vs. external dacryocystorhinostomy (ExDCR) in primarily acquired nasal duct obstruction. The search of PubMed, Embase, and Cochrane Central Register of Controlled Trials databases revealed 109 studies on ELDCR and ExDCR. Eleven studies were found to be suitable for review. The primary objective was to compare the success rate between ELDCR and ExDCR. The secondary objectives were to analyze the surgical time, overall complications, bleeding, infection, intranasal synechia, and granulation tissue. Pooled analysis of all studies revealed that ELDCR had a significantly lesser success rate compared to ExDCR (80.3% vs. 91.6%; odds ratio [OR] 0.41; 95% confidence interval [CI] [0.27, 0.62]; P < 00001; I2 = 13%). However, there were no difference in the overall complication rate (12.0% vs. 13.0%; OR 1.04; 95% CI [0.17, 6.33]; P = 0.97, I2 = 80%) and intranasal synechiae (9.5% vs. 4.3%; OR 2.22 [1.04, 4.72]; P = 0.04; I2 = 10%). The ExDCR group had significantly increased risks of bleeding (1.9% vs. 13.0%; OR 0.20; 95% CI [0.09, 0.47]; P = 0.0002; I2 = 0%) and infection (0.3% vs. 4.6%; OR 0.09; 95%CI [0.02, 0.51]; P = 0.006; I2 = 0%). Nevertheless, ELDCR needed a shorter surgical time compared to ExDCR (mean difference [MD] -28.35, 95% CI [-35.45, -21.26], P < 0.00001, I2 = 78%). Although ELDCR is associated with lesser bleeding, lesser infection, and shorter surgical duration, the success rate of ExDCR is higher.

Volumes of cochlear nucleus regions in rodents.

The cochlear nucleus receives all the coded information about sound from the cochlea and is the source of auditory information for the rest of the central auditory system. As such, it is a critical auditory nucleus. The sizes of the cochlear nucleus as a whole and its three major subdivisions - anteroventral cochlear nucleus (AVCN), posteroventral cochlear nucleus (PVCN), and dorsal cochlear nucleus (DCN) - have been measured in a large number of mammals, but measurements of its subregions at a more detailed level for a variety of species have not previously been made. Size measurements are reported here for the summed granular regions, DCN layers, AVCN, PVCN, and interstitial nucleus in 15 different rodent species, as well as a lagomorph, carnivore, and small primate. This further refinement of measurements is important because the granular regions and superficial layers of the DCN appear to have some different functions than the other cochlear nucleus regions. Except for DCN layers in the mountain beaver, all regions were clearly identifiable in all the animals studied. Relative regional size differences among most of the rodents, and even the 3 non-rodents, were not large and did not show a consistent relation to their wide range of lifestyles and hearing parameters. However, the mountain beaver, and to a lesser extent the pocket gopher, two rodents that live in tunnel systems, had relative sizes of summed granular regions and DCN molecular layer distinctly larger than those of the other mammals. Among all the mammals studied, there was a high correlation between the size per body weight of summed granular regions and that of the DCN molecular layer, consistent with other evidence for a close relationship between granule cells and superficial DCN neurons.

Effect of intranasal fluticasone furoate and intraocular olopatadine on nasal and ocular allergen-induced symptoms.

BACKGROUND: Nasal allergen challenge (NAC) leads to a nasal ocular reflex, which is augmented by allergic inflammation. This study was designed to confirm our previous observation that an intranasal steroid inhibits the nasal ocular reflex and to show that histamine does not play an important role in the genesis of this reflex. METHODS: We performed a randomized, double-blind, double-dummy, placebo (PL)-controlled, four-way crossover trial in subjects with seasonal allergic rhinitis out of season. Subjects were randomized to receive 1 week pretreatment with intranasal PL and intraocular (PL/PL), intranasal PL and intraocular olopatadine (PL/OLO), intranasal fluticasone furoate (FF) and intraocular PL (FF/PL), and the combination (FF/OLO). Subjects then underwent NAC on 2 consecutive days. The number of sneezes and nasal and ocular symptoms were recorded, and levels of tryptase and histamine were measured in nasal lavages. RESULTS: NAC after PL/PL resulted in increase in symptoms, histamine, and tryptase after the challenge on the 2nd day. There was a reduction in eye symptoms on the 2nd day of challenge from 6.0 after PL/PL to 0 after FF/PL (p = 0.001), 2.5 after PL/OLO (p = 0.3), and 1.5 after FF/OLO (p = 0.003). Furthermore, there was no significant difference between the response after FF/PL versus FF/OLO and a significant difference between FF/PL and PL/OLO (p = 0.02). Levels of tryptase followed a similar trend. The number of eosinophils in nasal lavages on the 2nd day of challenge were also reduced by the treatment arms containing FF compared with PL. CONCLUSION: Our data confirm the existence of a nasal ocular reflex after NAC. OLO alone or the addition of OLO to FF does not impact ocular symptoms caused by the naso-ocular reflex, suggesting that mast cells are not activated to release histamine in the conjunctiva during this process.

EF24 induces G2/M arrest and apoptosis in cisplatin-resistant human ovarian cancer cells by increasing PTEN expression.

We report that EF24, a synthetic compound 3,5-bis(2-flurobenzylidene)piperidin-4-one, greatly inhibits cisplatin-resistant (CR) human ovarian cancer cell proliferation. The inhibitory effect of EF24 on cell proliferation is associated with G(2)/M phase cell cycle arrest and increased G(2)/M checkpoint protein (pp53, p53, and p21) levels. Within 24 h following treatment, EF24 induced apoptosis in CR cells. The apoptosis was partially blocked by the general caspase inhibitor z-VAD. Within 12 h, EF24 induced a membranous FasL expression, consistent with a substantial decrease in the Ser(473) and Thr(308) phosphorylation of Akt, a known negative regulator of FasL transcription. Also, EF24 activated the phosphorylated PTEN and marginally up-regulated total PTEN expression through the inhibition of ubiquitin-mediated PTEN degradation. Suppression of PTEN expression with siRNA significantly reduced the p53 and p21 levels and activated Akt phosphorylation at Ser(473) and Thr(308), resulting in decreased apoptosis and increased cell survival. On the other hand, overexpression of PTEN markedly induced apoptosis. Our results clearly suggested that EF24 induced significant increase in PTEN expression. The up-regulation of PTEN inhibited Akt and MDM2, which enhanced the level of p53, thereby inducing G(2)/M arrest and apoptosis. Therefore, EF24 appears to have a potential therapeutic role in human ovarian cancer through the activation of PTEN.

Curcumin induces G2/M arrest and apoptosis in cisplatin-resistant human ovarian cancer cells by modulating Akt and p38 MAPK.

Curcumin, a major active component of turmeric, is known to induce apoptosis in several types of cancer cells, but little is known about its activity in chemoresistant cells. Hence, the aim of the present study was to investigate the anticancer properties of curcumin in cisplatin-resistant human ovarian cancer cells in vitro. The results indicated that curcumin inhibited the proliferation of both cisplatin-resistant (CR) and sensitive (CS) human ovarian cancer cells almost equally. Enhanced superoxide generation was observed in both CR and CS cells treated with curcumin. Curcumin induced G(2)/M phase cell-cycle arrest in CR cells by enhancing the p53 phosphorylation and apoptosis through the activation of caspase-3 followed by PARP degradation. Curcumin also inhibited the phosphorylation of Akt while the phosphorylation of p38 MAPK was enhanced. In summary, our results showed that curcumin inhibits the proliferation of cisplatin-resistant ovarian cancer cells through the induction of superoxide generation, G(2)/M arrest, and apoptosis.