Acquired or inherited or photoreceptor loss causes retinal ganglion cell loss and ultimately axonal transport alteration. Thus, therapies should be applied early during photoreceptors degeneration before the remodeling process reaches the inner retina. This study aimed to evaluate the protective effect of metformin on the rat optic nerve following photoreceptors loss induced by N-Ethyl-N-nitrosourea (ENU). Eighteen adults male Wistar rats were divided into two groups. Group I: normal vehicle control (n=6). Group II: ENU-induced photoreceptors degeneration (n=12) received a single intraperitoneal injection of ENU at a dose of 600 mg/kg. Rats in group II were equally divided into two subgroups:IIa: photoreceptor degeneration induced group and IIb: metformin treated group (200 mg/kg) for 7 days. Specimens from the optic nerve were processed for light and electron microscopy. In ENU treated group, the optic nerve revealed reduction in the diameter of the optic nerve fibers and thinning of myelin sheath with morphological changes in the glia (astrocytes, oligodendrocytes, and microglia). Caspase-3 (apoptotic marker), iNOS (oxidative stress marker) and CD68 (macrophage marker) expression increased. In metformin-treated group, the diameter of optic nerve fibers and myelin sheath thickness increased with improvement of the deterioration in the glia. Caspase-3, iNOS and CD68 expression decreased. Metformin ameliorates the histological changes of the rat optic nerve following photoreceptors loss induced by ENU.

Acquired or inherited or photoreceptor loss causes retinal ganglion cell loss and ultimately axonal transport alteration. Thus, therapies should be applied early during photoreceptors degeneration before the remodeling process reaches the inner retina. This study aimed to evaluate the protective effect of metformin on the rat optic nerve following photoreceptors loss induced by N-Ethyl-N-nitrosourea (ENU). Eighteen adults male Wistar rats were divided into two groups. Group I: normal vehicle control (n=6). Group II: ENU-induced photoreceptors degeneration (n=12) received a single intraperitoneal injection of ENU at a dose of 600 mg/kg. Rats in group II were equally divided into two subgroups:IIa: photoreceptor degeneration induced group and IIb: metformin treated group (200 mg/kg) for 7 days. Specimens from the optic nerve were processed for light and electron microscopy. In ENU treated group, the optic nerve revealed reduction in the diameter of the optic nerve fibers and thinning of myelin sheath with morphological changes in the glia (astrocytes, oligodendrocytes, and microglia). Caspase-3 (apoptotic marker), iNOS (oxidative stress marker) and CD68 (macrophage marker) expression increased. In metformin-treated group, the diameter of optic nerve fibers and myelin sheath thickness increased with improvement of the deterioration in the glia. Caspase-3, iNOS and CD68 expression decreased. Metformin ameliorates the histological changes of the rat optic nerve following photoreceptors loss induced by ENU.

BACKGROUND: Alkali-burned corneas can seldom heal properly to restore corneal transparency. Treatment of this severe disorder of the ocular surface remains a challenge. AIM OF THE WORK: was to investigate whether systemically transplanted bone marrow mesenchymal stem cells (BM-MSCs) can promote corneal wound healing after alkali burn. MATERIAL AND METHODS: Thirty five male New Zealand rabbits were used in this study. The animals were divided into three groups. Group I; the control group was sham operated. Group II; corneal alkali burn was created. Group III; underwent corneal alkali burn then treated with BM-MSCs. All corneas were collected after fourteen and twenty eight days. Evaluation using H&E, PAS & alkaline phosphatase reaction was carried out. Immune histo-chemical staining for CD44 and vimentin was performed as well. RESULTS: the corneal epithelium of (Group II) showed marked alterations. Vascularization, cellular infiltration and irregularity of the collagen fibers were also seen in the substantia propria. Increase in the thickness of the Descemet's membrane was noticed as well. On the other hand, at the time of 28 days, Group III rabbits showed best histological results with nearly healed corneas compared to other groups. Meanwhile, vimentin was more strongly expressed in Group III assessing the differentiating ability of BM-MSCs. CONCLUSION: BM-MSCs could effectively promote corneal alkali burn healing.
Alkalies* ; Alkaline Phosphatase ; Animals ; Bone Marrow* ; Burns* ; Collagen ; Cornea ; Descemet Membrane ; Epithelium, Corneal ; Hand ; Humans ; Male ; Mesenchymal Stem Cell Transplantation* ; Mesenchymal Stromal Cells ; Rabbits ; Vimentin ; Wound Healing

This systematic review evaluates current evidence regarding the feasibility of using needleless jet injection instead of a conventional local anesthetic needle. EBSCO, ProQuest, PubMed, and Scopus databases were used to identify relevant literature published in English from 2005 to 2020. Ten studies were selected. Five of them were randomized clinical trials, 3 case-control studies, and 2 equivalence trials. Using the Critical Appraisal Skills Program checklist, 6 studies scored between 67% and 100%, and 4 studies scored between 34% and 66%. According to Jadad’s scale, 2 studies were considered strong, and 8 studies were considered moderate in quality. The results of the 10 studies showed differences in patient preference for needleless jet injection. Needleless injection technique has been found to be particularly useful in uncooperative patients with anxiety and needle phobia.Needleless jet injection is not technique sensitive. However, with needleless jet anesthesia, most treatments require additional anesthesia. Conventional needle anesthesia is less costly, has a longer duration of action, and has better pain control during dental extraction. Needleless jet anesthesia has been shown to be moderately accepted by patients with a fear of needles, has a faster onset of action, and is an efficient alternative to conventional infiltration anesthesia technique.