Gideon Rosenthal

Overexpression of p53 tumor suppressor gene in pterygia.

Purpose To assess p53 gene expression in pterygia with and without recurrence. The pathogenesis of pterygium has not yet been determined. The most widely recognized etiologic factor is ultraviolet radiation, which leads to degeneration of the conjunctiva. However, pterygium was recently found to have several tumor-like characteristics. The p53 gene is a common marker for neoplasia, and is known to control cell cycle, cell differentiation and apoptosis. In this study we examined the expression of the p53 gene in primary pterygia with and without recurrence, searching for the pathogenesis of this very common lesion and for a prognostic factor for recurrence.Methods Immunohistochemical staining using a monoclonal antibody to human p53 (DO-7) was performed on 13 consecutive patients with primary pterygia, four pterygia without recurrence and nine pterygia which recurred during a 12-month follow-up. As a control we used two specimens of normal conjunctiva.Results Seven of the 13 pterygia specimens (54%) were positive for abnormal p53 expression. There was no difference between the groups with and without recurrence. Two out of four pterygia (50%) without recurrence and five out of nine (55.5%) pterygia with recurrence were positive. No pathological staining was observed in the control specimens.Conclusions In this study, abnormal p53 expression was found in pterygial epithelium, suggesting that pterygium could be a result of uncontrolled cell proliferation, and not as a degenerative lesion. There seems to be no connection between abnormal p53 expression and recurrence.

High Postdialysis Urea Rebound Can Predict Intradialytic Increase in Intraocular Pressure in Dialysis Patients with Lowered Intradialytic Hemoconcentration

Background: Intradialytic (ID) decrease in intraocular pressure (IOP) parallel to ultrafiltration-induced hemoconcentration has been recently reported. However, exacerbation of glaucoma in hemodialysis (HD) patients during HD sessions is occasionally observed. Postdialysis urea rebound (PDUR) is induced by the lag in urea removal from the cells to urea removal from the extracellular fluid, which when increased can result in ID drag of water to intracellular compartment. It is our hypothesis that similar lag in urea removal from ocular compartments may also be reflected by PDUR, and may induce drag of water into ocular compartments counteracting the effect of hemoconcentration. Our assumption was, therefore, that PDUR might predict ID increase in IOP. Methods: IOP, serum urea and hematocrit levels were measured at the start, end and 1 h postdialysis, in 19 chronic HD patients with normal IOP. Results: PDUR was positively correlated with mean (both eyes) ID changes in IOP (MIDIOP) (r = 0.5, p = 0.03) and % MIDIOP (r = 0.55, p = 0.02). ID increase in IOP was observed only in the 7 patients with relatively higher PDUR (≧9 mg%), who had also a relatively lower % ID change in Hct (<8%). MIDIOP was negatively correlated with % ID changes in Hct (r = –0.65, p = 0.03) in the 12 patients with PDUR ≧9 mg, and positively correlated with PDUR (r = 0.57, p = 0.03) in the 14 patients with % ID change in Hct <8%. Conclusion: High PDUR may predict susceptibility to ID increase in IOP in patients with lowered ID hemoconcentration.

Argon green laser photoepilation in the treatment of trachomatous trichiasis

Summary We describe the treatment of focal trachomatous trichiasis with argon green laser. We treated 70 eyelashes in 17 patients with 80% success and found this treatment modality convenient both for the patient and the practitioner.

Toxic effects of subconjunctival 5-fluorouracil and mitomycin C on ciliary body of rats.

Purpose: The effects of subconjunctival injection of mitomycin C and different concentrations of 5-fluorouracil on the epithelium of the ciliary body of twenty Sprague Dawley SD rats was studied.Methods: Twenty rats were divided into four treatment groups.The first three groups received 0.2 ml of 5, 10, and 30 mg of 5-fluorouracil subconjunctivally respectively, and the fourth group 0.2 ml of 0.4 mg/ml mitomycin C subconjunctivally. The right eye received 0.2 ml of the antimetabolite,while the left eye was injected with 0.2 ml of saline subconjunctivally, as a control.The eyes were examined histologically, in a masked fashion, by light and bytransmission electron microscopy. In each treatment group, two eyes were examined after one week, and three eyes were examined one month after the subconjunctival injection. Results: Electron microscopy revealed toxic effects in the epitheliumof the ciliary body of all treatment groups. The 5-fluorouracil group revealed focal mitochondrial edema, enlargement of intercellular spaces, and dilatation of intracellular spaces. The mitomycin C group showed pyknotic nuclei,enlargement of intercellular spaces, and irregular flattened epithelial cells. Theseverity of changes correlated with concentration and length of exposure. No pathology was found by light microscopy in all groups.Conclusions: This study demonstrates that subconjunctival antimetabolites mitomycin C and 5-fluorouracil can penetrate the sclera and exert toxiceffects on the epithelium of the ciliary body, even in low doses. These changeswere only apparent by electron microscopy and were still present one month after theinjection. These findings may contribute to the theory that the application ofantimetabolites during or after surgery has a direct effect on the epithelium of the ciliary body, besides its known effect on the conjunctiva. Further studies are needed to evaluate its effect on intraocular pressure.

Branch retinal vein occlusion in Churg−Strauss syndrome

The case is reported of a 64‐year‐old man who was diagnosed as having Churg−Strauss syndrome associated with branch retinal vein occlusion, without accompanying retinal vasculitis. It was assumed that the blood thrombocytosis caused a hypercoagulable state and thromboembolism leading to the branch retinal vein occlusion.

Adolescent Tuning of Association Cortex in Human Structural Brain Networks

Abstract Motivated by prior data on local cortical shrinkage and intracortical myelination, we predicted age-related changes in topological organization of cortical structural networks during adolescence. We estimated structural correlation from magnetic resonance imaging measures of cortical thickness at 308 regions in a sample of N = 297 healthy participants, aged 14–24 years. We used a novel sliding-window analysis to measure age-related changes in network attributes globally, locally and in the context of several community partitions of the network. We found that the strength of structural correlation generally decreased as a function of age. Association cortical regions demonstrated a sharp decrease in nodal degree (hubness) from 14 years, reaching a minimum at approximately 19 years, and then levelling off or even slightly increasing until 24 years. Greater and more prolonged age-related changes in degree of cortical regions within the brain network were associated with faster rates of adolescent cortical myelination and shrinkage. The brain regions that demonstrated the greatest age-related changes were concentrated within prefrontal modules. We conclude that human adolescence is associated with biologically plausible changes in structural imaging markers of brain network organization, consistent with the concept of tuning or consolidating anatomical connectivity between frontal cortex and the rest of the connectome.

Acetaminophen (paracetamol) levels in human tears

This study was designed to measure acetaminophen (paracetamol) levels in tears, and to compare it to serum levels. Paracetamol levels were measured in 20 paired tears and serum samples from 10 healthy volunteers, 1 and 2 hours after ingesting 1.5 g paracetamol. Tears were collected using glass microcapillary tubes while stimulating the conjunctiva with a small sponge placed in the lower fornix. Blood samples were taken simultaneously. The samples were analyzed for paracetamol levels using homogeneous enzyme immunoassay. Tears and serum paracetamol levels 1 hour after ingestion were 16.3 microg/mL +/- 7.2 (mean +/- SD), and 21.4 microg/mL +/- 7.7 (mean +/- SD) respectively. Tears and serum levels 2 hours after ingestion were 14.4 microg/mL +/- 7.8 (mean +/- SD), and 17 microg/mL +/- 7.6 (mean +/- SD) respectively. Tears and serum paracetamol levels of all the 20 paired samples (1 h and 2 h after ingestion) were 15.35 microg/mL +/- 7.4, and 19.25 microg/mL +/- 7.8, respectively (mean +/- SD). There was a strong and highly significant correlation between paracetamol levels in serum and in tears 1 and 2 hours after ingestion (r = 0.8, p = 0.005, r = 0.85, p = 0.002 respectively). Mean +/- SD ratio of tears/serum paracetamol levels 1 hour and 2 hours after ingestion were 0.77 +/- 0.21 and 0.81 +/- 0.25 respectively. Delta tears (difference in mean levels at 1 and 2 hours) paracetamol levels is significantly correlated with delta serum levels (r = 0.7, p = 0.025). A reliable, convenient, and feasible noninvasive method is described for measuring paracetamol in tears. There is no information in the literature about tears paracetamol secretion, and little information of tears drugs concentration.

Altered topology of neural circuits in congenital prosopagnosia

Using a novel, fMRI-based inter-subject functional correlation (ISFC) approach, which isolates stimulus-locked inter-regional correlation patterns, we compared the cortical topology of the neural circuit for face processing in participants with an impairment in face recognition, congenital prosopagnosia (CP), and matched controls. Whereas the anterior temporal lobe served as the major network hub for face processing in controls, this was not the case for the CPs. Instead, this group evinced hyper-connectivity in posterior regions of the visual cortex, mostly associated with the lateral occipital and the inferior temporal cortices. Moreover, the extent of this hyper-connectivity was correlated with the face recognition deficit. These results offer new insights into the perturbed cortical topology in CP, which may serve as the underlying neural basis of the behavioral deficits typical of this disorder. The approach adopted here has the potential to uncover altered topologies in other neurodevelopmental disorders, as well. DOI: http://dx.doi.org/10.7554/eLife.25069.001

Late Horner's syndrome following the bite of a black widow spider.

In this paper, we report on the case of a 23-year-old man who presented with a ptosis of the right upper lid and a miosis 1 month after being bitten in his right hand by Latrodectus revivenis. A positive cocaine test confirmed a diagnosis of Horners syndrome.

A possible neuronal account for the behavioural heterogeneity in congenital prosopagnosia

The extensive review paper by Geskin and Behrmann (Geskin & Behrmann, 2017) provides a survey of the behavioral literature of congenital prosopagnosia accumulated over the past years. The main goal of this survey is to address a longstanding debate in the cognitive neuroscience literature pertaining to the extent to which face and object processing share the same cognitive and neural mechanisms. Congenital prosopagnosia provides a unique testbed in which this issue can be addressed, given the well-documented core deficit in face processing and the absence of an apparent lesion, in contrast to cases of acquired prosopagnosia (Grill-Spector, Weiner, Kay, & Gomez, 2017). The main outcome of this review is that roughly two-thirds of the documented individuals diagnosed with CP also appear to have an impairment in object processing. This is somewhat surprising, given that despite the lack of formal behavioral and/or neural diagnostic criteria, most researchers would agree that CP is primarily considered a deficit in face processing. Yet, about a third of the reviewed cases exhibit a deficit which is confined to the domain of faces. Carving the behavioral variability associated with CP is of great importance as it enables deeper understanding of the mechanisms underlying the impairment. Moreover, these findings also have general implications for our understanding of normal face and object representation in the human brain. Beyond the cognitive level, the findings also raise questions regarding the neural models that could underlie such behavioral heterogeneity. Specifically, what would be the most parsimonious neural mechanism that could simultaneously account for such different behavioral profiles? A deficit affecting both face and object processing, as found in two-thirds of the CP participants, is compatible with a system associated with more general, high-level visual processing. In contrast, a deficit that is restricted to faces and does not extend to other visual domains, as observed in the remaining third, is more compatible with a modular dual system organization in which faces and objects are processed by separate systems. How could one reconcile these different behavioral profiles within a single neural model and a single disorder? Normal face recognition appears to be accomplished via the coordinated activity of multiple nodes of a distributed neural network (see GrillSpector et al., 2017, for a recent review). Hence, a number of studies in recent years, including our own (Rosenthal, Sporns, & Avidan, 2017), have begun to adopt a network methodology and framework to better characterize the functional aspects of this system. According to this approach, the totality of the network connections and interactions can be summarized and systematically analyzed using concepts of network science. In general, networks comprise a set of elements (i.e., nodes) and their dyadic (pairwise) connections (i.e., edges), which permit the characterization of each element’s connection pattern and topology (Bullmore & Sporns, 2009). Within this framework, the study of individuals with CP provides the opportunity to determine whether a disrupted function of one or more of the nodes or edges within this network leads to an altered