Efficacy of artificial tears containing trehalose and hyaluronic acid for dry eye disease in women aged 42-54 versus ≥ 55 years.

BACKGROUND AND OBJECTIVES: Dry eye disease (DED) is common in postmenopausal women. This study evaluated efficacy of a 3-month daily treatment with artificial tears containing trehalose and hyaluronic acid (HA) in women aged 42-54 years (mixed-hormonal status) versus ≥ 55 years (postmenopausal) and with moderate and severe DED. METHODS: This was a post-hoc analysis of three clinical trials assessing the efficacy of artificial tears containing trehalose (3%) and HA (0.15%) in women with an Ocular Surface Disease Index (OSDI) ≥ 18. Patients instilled one drop of the artificial tears in each eye 3 to 6 times daily and were evaluated at baseline and after 84 ± 7 days for DED symptom severity (OSDI), hyperemia (McMonnies scale), tear break-up time (TBUT), corneal and conjunctival staining (Oxford and Van Bjisterveld scales), tear production (Schirmer I test), and ocular symptoms. RESULTS: A total of 273 women were evaluated, 61 of age 42-54 years; 212 of ≥ 55 years. DED symptoms, as measured by the OSDI, decreased significantly with the treatment in both age groups (p < 0.0001). Conjunctival hyperemia decreased significantly and TBUT increased significantly in both groups, especially in women of age 42-54 (both p < 0.0001). The global (corneal and conjunctival) staining score decreased significantly in both groups, but also more in women of age 42-54 years. No differences were observed between age groups for any of the variables measured, except for visual acuity. DED symptoms were consistently reported more frequently by the mixed hormonal status women, but also the effect of the treatment was more pronounced in this group. CONCLUSIONS: Artificial tears with trehalose and HA significantly improved the symptoms of DED in women aged 42-54 and ≥ 55 years. The decrease in symptoms was more pronounced in women of age 42-54 years, suggesting better mechanisms of recovery from inflammation and loss of ocular surface homeostasis.

TFOS European Ambassador meeting: Unmet needs and future scientific and clinical solutions for ocular surface diseases.

The mission of the Tear Film & Ocular Surface Society (TFOS) is to advance the research, literacy, and educational aspects of the scientific field of the tear film and ocular surface. Fundamental to fulfilling this mission is the TFOS Global Ambassador program. TFOS Ambassadors are dynamic and proactive experts, who help promote TFOS initiatives, such as presenting the conclusions and recommendations of the recent TFOS DEWS II™, throughout the world. They also identify unmet needs, and propose future clinical and scientific solutions, for management of ocular surface diseases in their countries. This meeting report addresses such needs and solutions for 25 European countries, as detailed in the TFOS European Ambassador meeting in Rome, Italy, in September 2019.

Connective tissue structure of the tree shrew optic nerve and associated ageing changes.

PURPOSE: To identify the structure and composition of the tree shrew optic nerve to determine its potential as a model for glaucoma. METHODS: Tree shrew optic nerves, aged 4 weeks to 5 years, were wax or cryoembedded for analysis of overall morphology and cellular (glial fibrillary acidic protein [GFAP]) and extracellular matrix (collagen types I, III, IV, V, VI; fibronectin; and elastin) immunolocalization studies. In addition, transmission and scanning electron microscopy were performed. In vivo optic disc imaging was performed by HRT2 and fundus camera photography. RESULTS: The optic nerve of the tree shrew comprised regions comparable to the human prelaminar and lamina cribrosa (LC) in the optic nerve head and the retrolaminar region, immediately posterior. The multilayered connective tissue plates of tree shrew LC stretched across the optic nerve canal at the level of the sclera and consisted of collagen types I, III, IV, V, and VI; elastin; and fibronectin. Significant age-related alterations in connective tissue components were indicated. Connective tissue was present in the central retinal vessel sheaths and was identified as longitudinally oriented collagen fibrils in the retrolaminar optic nerve. GFAP immunofluorescence indicated a high concentration of astrocytic processes in the LC. Myelination of axons was evident in the retrolaminar optic nerve. Ultrastructural studies supported the structural organization and spatial distribution of connective tissue. CONCLUSIONS: In contrast to many rodent models of glaucoma, since the tree shrew optic nerve resembles that in humans, especially at the LC, the tree shrew offers an ideal opportunity to investigate glaucoma pathophysiology in a subprimate model.

The second galanin receptor GalR2 plays a key role in neurite outgrowth from adult sensory neurons.

Expression of the neuropeptide galanin is markedly upregulated within the adult dorsal root ganglion (DRG) after peripheral nerve injury. We demonstrated previously that the rate of peripheral nerve regeneration is reduced in galanin knock-out mice, with similar deficits observed in neurite outgrowth from cultured mutant DRG neurons. Here, we show that the addition of galanin peptide significantly enhanced neurite outgrowth from wild-type sensory neurons and fully rescued the observed deficits in mutant cultures. Furthermore, neurite outgrowth in wild-type cultures was reduced to levels observed in the mutants by the addition of the galanin antagonist M35 [galanin(1-13)bradykinin(2-9)]. Study of the first galanin receptor (GalR1) knock-out animals demonstrated no differences in neurite outgrowth compared with wild-type animals. Similarly, use of a GalR1-specific antagonist had no effect on neuritogenesis. In contrast, use of a GalR2-specific agonist had equipotent effects on neuritogenesis to galanin peptide, and inhibition of PKC reduced neurite outgrowth from wild-type sensory neurons to that observed in galanin knock-out cultures. These results demonstrate that adult sensory neurons are dependent, in part, on galanin for neurite extension and that this crucial physiological process is mediated by activation of the GalR2 receptor in a PKC-dependent manner.