Measurement of a novel optic disc topographic parameter, ”spikiness”, in glaucoma

Background: Structural changes in the lamina cribrosa have been implicated in the pathogenesis of glaucomatous optic atrophy, but not observed. This paper presents a novel parameter of topographic variability within the optic disc, termed ”spikiness”, which may reflect glaucoma-related changes in the lamina. Methods: Four age-matched groups of normal patients (n=12, mean age 64.8 years) and patients with ocular hypertension (n=14, mean age 63.1), primary open-angle glaucoma (n=11, mean age 70) and low-tension glaucoma (n=15, mean age 66.3) were recruited. Images of normal and glaucomatous eyes from the Heidelberg Retina Tomograph were imported into ERDAS image processing software where the spikiness data (30 consecutive mean surface height values across the base of the optic cup in both the vertical and horizontal meridians) were extracted in a format that facilitated further statistical analysis. Results: Significant differences in topographic variability (spikiness) existed in the vertical (F=3.64, P=0.01) but not the horizontal meridian (F=1.25, P=0.3) through the optic disc. Spikiness was inversely related to Humphrey mean deviation (P<0.05), and cup-disc ratio (P<0.004) and was directly related to nerve fibre layer thickness (P<0.005). Of particular interest was the finding that the spikiness measure was the only optic disc parameter to significantly discriminate low tension glaucoma from primary open angle glaucoma. Conclusion: A new measure of surface variability (topography) at the floor of the optic cup has been described. The new index of spikiness may represent a measurement of lamina cribrosa fragility which has been implicated, but not previously estimated, in glaucomatous eyes. Received: 6 January 2000 Revised: 27 March 2000 Accepted: 30 March 2000     

Diuretic resistant oedema: nailing the diagnosis.

Introduction Peripheral oedema is a commonly encountered clinical problem.Although it has many causes, its pathophysiology ultimatelyinvolves two processes: altered capillary haemodynamics andrenal salt and water retention. A minority of cases are resistantto diuretic treatment; causes of such resistance include excessivesodium intake, poor diuretic drug absorption, reduced secretionof free diuretic into urine (for example, in nephrotic syndrome,renal failure, and heart failure), and lymphatic obstruction.We present a case of diuretic-resistant oedema associated withpleural and pericardial effusions. Only after extensive ‘negative’     

Anal sphincter injury in vaginal deliveries complicated by shoulder dystocia

Introduction and hypothesis

Shoulder dystocia is an obstetric emergency that occurs in 0.2–3% of all cephalic vaginal deliveries. We hypothesized that because of the difficult nature of deliveries complicated by shoulder dystocia, the condition may be associated with anal sphincter injury. We sought to identify risk factors for obstetric anal sphincter injury in women with shoulder dystocia.

Methods

This retrospective analysis included all cases of shoulder dystocia from 2007 to 2011 at two large tertiary referral centers, in the USA and Ireland. Details of maternal demographics, intrapartum characteristics, and delivery outcomes in cases of shoulder dystocia were analyzed. Univariate and multivariate analyses were used to describe the association between shoulder dystocia and anal sphincter injury.

Results

There were 685 cases of shoulder dystocia, and the rate of shoulder dystocia was similar at both institutions. The incidence of anal sphincter injury was 8.8% (60 out of 685). The rate was 14% (45 out of 324) in nulliparas and 4.2% (15 out of 361) in multiparas. Women with sphincter injury were more likely to be nulliparous (75% [45 out of 60] vs 45% [279 out of 625]; p < 0.0001), have had an operative vaginal delivery (50% [30 out of 60] vs 36% [226 out of 625]; p = 0.03) and require internal maneuvers (50% [30 out of 60] vs 32% [198 out of 625], p = 0.004) than those with an intact sphincter. On multivariate regression analysis, these predictors of sphincter injury remained significant when adjusted for other risk factors. Episiotomy was negatively associated with sphincter injury on multivariate regression analysis.

Conclusions

In a retrospective cohort of 685 women with shoulder dystocia, the risk of anal sphincter injury is 9%. Risk factors include nulliparity, operative vaginal delivery, and use of internal maneuvers, whereas episiotomy was found to have a protective effect against anal sphincter injury during cases of shoulder dystocia.

     

Is the P300 wave an endophenotype for schizophrenia? A meta-analysis and a family study

INTRODUCTION: We assessed the usefulness of the P300 wave as endophenotype for schizophrenia by means of a meta-analysis of the literature as well as our own family study. METHOD: Meta-analysis: We conducted a systematic search for articles published between 1983 and 2003 that reported P300 measures in non-psychotic relatives of schizophrenic patients and in healthy controls. Meta-regression analyses were performed using a random effects procedure. The pooled standardized effect size (PSES) was calculated as the difference between the means of the two groups divided by the common standard deviation. Local study: We examined the P300 wave with a standard two-tone oddball paradigm in 30 patients with schizophrenia, 40 non-psychotic relatives, and 40 controls using linear mixed models. RESULTS: Meta-analysis: We pooled 472 relatives and 513 controls. The P300 amplitude was significantly reduced in relatives (PSES = 0.61; 95% CI: 0.30 to 0.91; P < 0.001). The P300 latency was significantly delayed in relatives (PSES of -0.50; 95% CI: -0.88 to -0.13; P = 0.009]. Local study: The patients showed a trend for amplitude reductions (P = 0.06) and significant latency delays (P < 0.01). The relatives displayed normal amplitude but had significant latency delays (P = 0.01). The P300 amplitude and especially the P300 latency are promising alternative phenotypes for genetic research into schizophrenia.     

Preferential tendon stem cell response to growth factor supplementation

Tendon injuries are increasingly prevalent around the world, accounting for more than 100 000 new clinical cases/year in the USA alone. Cell‐based therapies have been proposed as a therapeutic strategy, with recent data advocating the use of tendon stem cells (TSCs) as a potential cell source with clinical relevance for tendon regeneration. However, their in vitro expansion is problematic, as they lose their multipotency and change their protein expression profile in culture. Herein, we ventured to assess the influence of insulin‐like growth factor 1 (IGF‐1), growth and differentiation factor‐5 (GDF‐5) and transforming growth factor‐β1 (TGFβ1) supplementation in TSC culture. IGF‐1 preserved multipotency for up to 28 days. Upregulation of decorin and scleraxis expression was observed as compared to freshly isolated cells. GDF‐5 treated cells exhibited reduced differentiation along adipogenic and chondrogenic pathways after 28 days, and decorin, scleraxis and collagen type I expression was increased. After 28 days, TGFβ1 supplementation led to increased scleraxis, osteonectin and collagen type II expression. The varied responses to each growth factor may reflect their role in tendon repair, suggesting that: GDF‐5 promotes the transition of tendon stem cells towards tenocytes; TGFβ1 induces differentiation along several pathways, including a phenotype indicative of fibrocartilage or calcified tendon, common problems in tendon healing; and IGF‐1 promotes proliferation and maintenance of TSC phenotypes, thereby creating a population sufficient to have a beneficial effect. Copyright © 2014 John Wiley & Sons, Ltd.