Effects of Merogel coverage on wound healing and ostial patency in endonasal endoscopic dacryocystorhinostomy for primary chronic dacryocystitis

Purpose: To investigate the effects of Merogel coverage on ostial patency in endonasal endoscopic dacryocystorhinostomy (EES-DCR) for primary chronic dacryocystitis (PCD). Methods: In all, 260 patients with unilateral PCD were randomized into two groups: the Merogel group and the control group. All patients underwent EES-DCR. The Merogel group received Merogel covering the wound 1–2 mm around the ostium and the control group received no treatment. Patients were followed up for 9 months. The mucosal epithelialization of the wound, the proliferation of fibrosis tissue, and the success rate of ostial patency were compared. Results: Our study included 112 patients in the Merogel group and 115 patients in the control group. At the 2-week review, intact mucosal epithelium lined the ostia in 96 Merogel patients compared with 80 control patients (ITT analysis: χ ²=4.502, P=0.034). At the 9-month review, scars were present in 18 patients in the Merogel group compared with 39 patients in the control group (ITT analysis: χ ²=9.909, P=0.002, ITT analysis). No differences were observed in the granulation formation between the two groups. The success rate of ostial patency reached 94.6% (106/112) in the Merogel group compared with 80% (92/115) in the control group (ITT analysis: χ ²=4.151, P=0.042). Conclusion: Merogel coverage may enhance the success rate of EES-DCR for PCD by promoting mucosal epithelial healing and preventing excessive scarring.W Wu, PS Cannon, W Yan, Y Tu, D Selva and J Q

Survey of Selective Neurotoxins

There has been an awareness of nerve poisons from ancient times. At the dawn of the twentieth century, the actions and mechanisms of these poisons were uncovered by modern physiological and biochemical experimentation. However, the era of selective neurotoxins began with the pioneering studies of R. Levi-Montalcini through her studies of the neurotrophin nerve growth factor (NGF), a protein promoting growth and development of sensory and sympathetic noradrenergic nerves. An antibody to NGF, namely, anti-NGF - developed in the 1950s in a collaboration with S. Cohen - was shown to produce an immunosympathectomy and virtual lifelong sympathetic denervation. These Nobel Laureates thus developed and characterized the first identifiable selective neurotoxin. Other selective neurotoxins were soon discovered, and the compendium of selective neurotoxins continues to grow, so that today there are numerous selective neurotoxins, with the potential to destroy or produce dysfunction of a variety of phenotypic nerves. Selective neurotoxins are of value because of their ability to selectively destroy or disable a common group of nerves possessing (1) a particular neural transporter, (2) a unique set of enzymes or vesicular transporter, (3) a specific type of receptor or (4) membranous protein, or (5) other uniqueness. The era of selective neurotoxins has developed to such an extent that the very definition of a selective neurotoxin has warped. For example, (1) N-methyl-D- aspartate receptor (NMDA-R) antagonists, considered to be neuroprotectants by virtue of their prevention of excitotoxicity from glutamate receptor agonists, actually lead to the demise of populations of neurons with NMDA receptors, when administered during ontogenetic development. The mere lack of natural excitation of this nerve population, consequent to NMDA-R block, sends a message that these nerves are redundant - and an apoptotic cascade is set in motion to eliminate these nerves. (2) The rodenticide rotenone, a global cytotoxin that acts mainly to inhibit complex I in the respiratory transport chain, is now used in low dose over a period of weeks to months to produce relatively selective destruction of substantia nigra dopaminergic nerves and promote alpha-synuclein deposition in brain to thus model Parkinson\u27s disease. Similarly, (3) glial toxins, affecting oligodendrocytes or other satellite cells, can lead to the damage or dysfunction of identifiable groups of neurons. Consequently, these toxins might also be considered as selective neurotoxins, despite the fact that the targeted cell is nonneuronal. Likewise, (4) the dopamine D2-receptor agonist quinpirole, administered daily for a week or more, leads to development of D2-receptor supersensitivity - exaggerated responses to the D2-receptor agonist, an effect persisting lifelong. Thus, neuroprotectants can become selective neurotoxins; nonspecific cytotoxins can become classified as selective neurotoxins; and receptor agonists, under defined dosing conditions, can supersensitize and thus be classified as selective neurotoxins. More examples will be uncovered as the area of selective neurotoxins expands. The description and characterization of selective neurotoxins, with unmasking of their mechanisms of action, have led to a level of understanding of neuronal activity and reactivity that could not be understood by conventional physiological observations. This chapter will be useful as an introduction to the scope of the field of selective neurotoxins and provide insight for in-depth analysis in later chapters with full descriptions of selective neurotoxins

ESICM LIVES 2016: part two : Milan, Italy. 1-5 October 2016.

Meeting abstrac