The Outcome of Photo-Therapy on Serum Calcium Values in Term Neonates: A Cross Sectional Study

Background: In the management of hyperbilirubinemia in neonates, phototherapy is an important treatment modality. Photo-therapy can cause skin rashes, diarrhoea, increase in body temperature, retinal damage and bronze baby syndrome. Photo-therapy is thought to influence serum calcium levels by inhibiting pineal melatonin secretion. Aims and Objectives: The aim of this research was to see how photo-therapy affected serum calcium values in a term neonate. Materials and Methods: Over the course of six months, 74 neonates were studied in the neonatology department of a tertiary healthcare centre in Central India. Results: Calcium values fell in 77 % of the neonates in our sample, but only one case fell into significant symptomatic hypocalcemic range (1 percent). Conclusion: According to the findings, neonates who are receiving photo-therapy have a higher risk of falling into the hypocalemic range. As a result, neonates should be strictly observed for calcium shifts and treated appropriately.

LightOCT: Exploring the depth for Retinal disease detection

With the advancement in technology and computation capabilities, identifying retinal damage through state-of-the-art CNNs architectures has led to the speedy and precise diagnosis, thus inhibiting further disease development. In this study, we focus on the classification of retinal damage caused by detecting choroidal neovascularization (CNV), diabetic macular edema (DME), DRUSEN, and NORMAL in optical coherence tomography (OCT) images. The emphasis of our experiment is to investigate the component of depth in the neural network architecture. We introduce a shallow convolution neural network - LightOCT, outperforming the other deep model configurations, with the lowest value of LVCEL and highest accuracy (+98\% in each class). Next, we experimented to find the best fit optimizer for LightOCT. The results proved that the combination of LightOCT and Adam gave the most optimal results. Finally, we compare our approach with transfer learning models, and LightOCT outperforms the state-of-the-art models in terms of computational cost, least training time and gives comparable results in the criteria of accuracy. We would direct our future work to improve the accuracy metrics with shallow models such that the trade-off between training time and accuracy is reduced.

Vitamin A cycle byproducts explain retinal damage and molecular changes thought to initiate retinal degeneration

ABSTRACT In the most prevalent retinal diseases, including Stargardt disease and age-related macular degeneration (AMD), byproducts of vitamin A form in the retina abnormally during the vitamin A cycle. Despite evidence of their toxicity, whether these vitamin A cycle byproducts contribute to retinal disease, are symptoms, beneficial, or benign has been debated. We delivered a representative vitamin A byproduct, A2E, to the rat's retina and monitored electrophysiological, histological, proteomic, and transcriptomic changes. We show that the vitamin A cycle byproduct is sufficient alone to damage the RPE, photoreceptor inner and outer segments, and the outer plexiform layer, cause the formation of sub-retinal debris, alter transcription and protein synthesis, and diminish retinal function. The presented data are consistent with the theory that the formation of vitamin A byproducts during the vitamin A cycle is neither benign nor beneficial but may be sufficient alone to cause the most prevalent forms of retinal disease. Retarding the formation of vitamin A byproducts could potentially address the root cause of several retinal diseases to eliminate the threat of irreversible blindness for millions of people.

Dpp/TGFβ-superfamily play a dual conserved role in mediating the damage response in the retina

Retinal homeostasis relies on intricate coordination of cell death and survival in response to stress and damage. Signaling mechanisms that coordinate this process in the adult retina remain poorly understood. Here we identify Decapentaplegic (Dpp) signaling in Drosophila and its mammalian homologue Transforming Growth Factor-beta (TGFβ) superfamily, that includes TGFβ and Bone Morphogenetic Protein (BMP) signaling arms, as central mediators of retinal neuronal death and tissue survival following acute damage. Using a Drosophila model for UV-induced retinal damage, we show that Dpp released from immune cells promotes tissue loss after UV-induced retinal damage. Interestingly, we find a dynamic response of retinal cells to this signal: in an early phase, Dpp-mediated stimulation of Saxophone/Smox signaling promotes apoptosis, while at a later stage, stimulation of the Thickveins/Mad axis promotes tissue repair and survival. This dual role is conserved in the mammalian retina through the TGFβ/BMP signaling, as supplementation of BMP4 or inhibition of TGFβ using small molecules promotes retinal cell survival, while inhibition of BMP negatively affects cell survival after light-induced photoreceptor damage and NMDA induced inner retinal neuronal damage. Our data identify key evolutionarily conserved mechanisms by which retinal homeostasis is maintained.

Human Umbilical Cord-Mesenchymal Stem Cells Survive and Migrate within the Vitreous Cavity and Ameliorate Retinal Damage in a Novel Rat Model of Chronic Glaucoma

Glaucoma is the leading cause of irreversible blindness worldwide, and pathologically elevated intraocular pressure (IOP) is the major risk factor. Neuroprotection is one of the potential therapies for glaucomatous retinal damage. Intravitreal mesenchymal stem cell (MSC) transplantation provides a viable therapeutic option, and human umbilical cord- (hUC-) MSCs are attractive candidates for cell-based neuroprotection. Here, we investigated the ability of transplanted hUC-MSCs to survive and migrate within the vitreous cavity and their neuroprotective effects on chronic glaucomatous retina. For this, we developed a chronic ocular hypertension (COH) rat model through the intracameral injection of allogeneic Tenon’s fibroblasts. Green fluorescent protein-transduced hUC-MSCs were then injected into the vitreous cavity one week after COH induction. Results showed that a moderate IOP elevation lasted for two months. Transplanted hUC-MSCs migrated toward the area of damaged retina, but did not penetrate into the retina. The hUC-MSCs survived for at least eight weeks in the vitreous cavity. Moreover, the hUC-MSCs were efficient at decreasing the loss of retinal ganglion cells; retinal damage was attenuated through the inhibition of apoptosis. In this study, we have developed a novel COH rat model and demonstrated the prolonged neuroprotective potential of intravitreal hUC-MSCs in chronic glaucoma.

Inflammation modulates regeneration in the acute or chronically damaged zebrafish retina

Unlike mammals, zebrafish regenerate in response to retinal damage. Because microglia are activated by retinal damage, we investigated their role during regeneration following acute or chronic damage. At three weeks-post-fertilization (wpf), fish exhibiting NMDA-induced acute damage or cone photoreceptor-specific chronic degeneration, the gold rush (gosh) mutant, displayed reactive microglia and Müller glia proliferation. Retinas treated to inhibit the immune response lacked reactive microglia and possessed fewer PCNA-positive cells, while LPS treatment increased microglia and PCNA-labeled cells. NMDA-injured retinas upregulated the expression of il-1β and tnf-α pro-inflammatory cytokine genes, followed by increased expression of il-10 and arg1 anti-inflammatory/remodeling cytokine genes. An early and transiently TNF-α pro-inflammatory microglia population was identified in the NMDA-damaged retina. In contrast, gosh mutant retinas exhibited a mild increase of pro-inflammatory cytokine gene expression concurrently with a greater increased in anti-inflammatory/remodeling cytokine gene expression. Few TNF-α pro-inflammatory microglia were observed in the gosh retina. How inflammation regulates regeneration in zebrafish would provide important clues towards improving the therapeutic strategies for repairing injured mammalian tissues.