Radiation Retinopathy: Case report and review

BACKGROUND: Ocular damage from radiation treatment is a well established phenomenon. Many factors are now known to influence the incidence of radiation retinopathy, including total dosage and daily fraction size. Patients who are diabetic, hypertensive or received previous chemotherapy are more susceptible to radiation retinopathy. CASE PRESENTATION: A 55 year old male was referred from the oncology department with epiphora. His medical history included Type 2 Insulin treated Diabetes Mellitus and hypertension. One year prior to presentation he had undergone a total rhinectomy with a 4 week course of post-operative radiotherapy for an aggressive sqaumous cell carcinoma of the nose. On examination the visual acuity was noted to be 6/36 left eye and 6/9 right eye. Posterior segment examination revealed marked retinal ischaemia present in the posterior pole and macular region of both eyes. The appearance was not thought to be typical of diabetic changes, radiation retinopathy being the more likely diagnosis especially in view of his history. Over the next four months the vision in both eyes rapidly deteriorated to 3/60 left eye and 1/60 right eye. Bilateral pan retinal photocoagulation was thought to be appropriate treatment at this point. CONCLUSION: This case highlights the importance for ophthalmologists and oncologists to be aware of the close relationship between diabetes and radiation treatment and the profound rapid impact this combination of factors may have on visual function. Radiation is being used with increasing frequency for ocular and orbital disease, because of this more cases of radiation retinopathy may become prevalent. Factors which may potentiate radiation retinopathy should be well known including, increased radiation dosage, increased fraction size, concomitant systemic vascular disease and use of chemotherapy. Counselling should be offered in all cases at risk of visual loss. As no effective treatment currently exists to restore visual function, monitoring of visual acuity in all cases and early referral to the ophthalmologist as appropriate is warranted

Zona Incerta Suppressed Escape During Hunger

Wild animals must avoid starvation and predators to survive. However, the motivation to seek food and shelter promote opposing behaviors and require rapid neural adaptations that are poorly understood. The zona incerta (ZI) is a specialized region that integrates multisensory input, projects strongly to motor-related regions, and can thus initiate escape from threats to survive. One subset of medial ZI neurons producing dopamine (DA) and gamma-aminobutyric acid (GABA) send dense projections to the medial motor-related superior colliculus (SCm), which promotes escape from threats in the upper visual field. We determined whether ZI-GABA/DA cells respond to hunger and investigated whether activating ZI-GABA/DA cells in hungry mice suppressed escape. We transduced ZI-GABA/DA cells with an excitatory chemogenetic receptor hM3(Dq) and found that stimulating their projections in the medial SCm suppressed escape from an upper visual threat in male and female mice. Interestingly, fasting activated ZI-GABA/DA cells and enhanced hM3(Dq)-mediated escape suppression. To evaluate the contribution of GABA and/or DA in escape suppression, we co-infused a cocktail of DA or GABA receptor antagonists, respectively. Both GABA and DA are required to suppress escape in fasted male mice, but DA independently suppressed escape in female mice. Activation of ZI-GABA/DA cells did not impact locomotor or any anxiety-related functions but uniquely integrated hunger signals to suppress escape. Our findings suggested that the ZI-SCm neurocircuit is sexually dimorphic and that the ZI is a critical node regulating the competition between the need to seek food and shelter

The Hidden Costs of Sweetness: Fructose-Induced Liver Inflammation

Fructose consumption has contributed to the prevalence of obesity, a major risk factor for metabolic disorders like metabolic-associated liver disease (MASLD). Obesity frequently coexists with liver disease, and excessive fructose intake directly promotes MASLD by driving hepatic inflammation, oxidative stress, and metabolic dysfunction. Despite growing research, gaps remain in understanding how dietary fructose leads to liver dysfunction. Many MASLD models rely on supraphysiological fructose levels (60%), which limit their relevance to the human diet. In this study, we investigated how dietary sugars at levels (15%) comparable to that in the Western diet influence liver health. To do so, we analyzed inflammatory, oxidative stress, and metabolic gene expression in mice-fed diets containing 15% fructose, 60% fructose, or standard chow.  We fed seventeen male and female mice sugar-based diets for 8 to 23 weeks and analyzed gene expression using quantitative PCR. Mice on 60% and 15% fructose diets showed comparable gene expression patterns, with Nrf2 and Cd36 displaying significant differences. When compared to other sugar types, dextrose and sucrose also induced the expression of similar inflammatory liver markers. Since a 60% fructose diet is known to induce MASLD, our results suggest that even 15% fructose may have similar effects. However, dextrose and sucrose increased both pro- and anti-inflammatory gene expression, making their role in MASLD unclear. These findings highlight the complex relationship between dietary sugars and liver health, emphasizing the need for further research on the long-term effects of different sugar types in MASLD development