Deep and Densely Connected Networks for Classification of Diabetic Retinopathy.

Diabetes has recently emerged as a worldwide problem, and diabetic retinopathy is an abnormal state associated with the human retina. Due to the increase in daily screen-related activities of modern human beings, diabetic retinopathy is more prevalent among adults, leading to minor and major blindness. Doctors and clinicians are unable to perform early diagnoses due to the large number of patients. To solve this problem, this study introduces a classification model for retinal images that distinguishes between the various stages of diabetic retinopathy. This work involves deploying deep and densely connected networks for retinal image analysis with training from scratch. Dense connections between the convolutional layers of the network are an essential factor to enhance accuracy owing to the deeper supervision between layers. Another factor is the growth rate that further assists our model in learning more sophisticated feature maps regarding retinal images from every stage of the network. We compute the area under the curve, sensitivity, and specificity, particularly for messidor-2 and EyePACS. Compared to existing approaches, our method achieved better results, with an approximate rise rate of 0.01, 0.03, and 0.01, respectively. Therefore, computer-aided programs can help in diagnostic centers as automated detection systems.

Heat stress enhances LTM formation in Lymnaea: role of HSPs and DNA methylation.

Environmentally relevant stressors alter the memory-forming process in Lymnaea following operant conditioning of aerial respiration. One such stressor is heat. Previously, we found that following a 1 h heat shock, long-term memory (LTM) formation was enhanced. We also had shown that the heat stressor activates at least two heat shock proteins (HSPs): HSP40 and HSP70. Here, we tested two hypotheses: (1) the production of HSPs is necessary for enhanced LTM formation; and (2) blocking DNA methylation prevents the heat stressor-induced enhancement of LTM formation. We show here that the enhancing effect of the heat stressor on LTM formation occurs even if snails experienced the stressor 3 days previously. We further show that a flavonoid, quercetin, which inhibits HSP activation, blocks the enhancing effect of the heat stressor on LTM formation. Finally, we show that injection of a DNA methylation blocker, 5-AZA, before snails experience the heat stressor prevents enhancement of memory formation.

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration.

Diabetic peripheral neuropathy affects up to half of diabetic patients. This neuronal damage leads to sensory disturbances, including allodynia and hyperalgesia. Many growth factors have been suggested as useful treatments for prevention of neurodegeneration, including the vascular endothelial growth factor (VEGF) family. VEGF-A is generated as two alternative splice variant families. The most widely studied isoform, VEGF-A165a is both pro-angiogenic and neuroprotective, but pro-nociceptive and increases vascular permeability in animal models. Streptozotocin (STZ)-induced diabetic rats develop both hyperglycaemia and many of the resulting diabetic complications seen in patients, including peripheral neuropathy. In the present study, we show that the anti-angiogenic VEGF-A splice variant, VEGF-A165b, is also a potential therapeutic for diabetic neuropathy. Seven weeks of VEGF-A165b treatment in diabetic rats reversed enhanced pain behaviour in multiple behavioural paradigms and was neuroprotective, reducing hyperglycaemia-induced activated caspase 3 (AC3) levels in sensory neuronal subsets, epidermal sensory nerve fibre loss and aberrant sciatic nerve morphology. Furthermore, VEGF-A165b inhibited a STZ-induced increase in Evans Blue extravasation in dorsal root ganglia (DRG), saphenous nerve and plantar skin of the hind paw. Increased transient receptor potential ankyrin 1 (TRPA1) channel activity is associated with the onset of diabetic neuropathy. VEGF-A165b also prevented hyperglycaemia-enhanced TRPA1 activity in an in vitro sensory neuronal cell line indicating a novel direct neuronal mechanism that could underlie the anti-nociceptive effect observed in vivo. These results demonstrate that in a model of Type I diabetes VEGF-A165b attenuates altered pain behaviour and prevents neuronal stress, possibly through an effect on TRPA1 activity.

What's hot: the enhancing effects of thermal stress on long-term memory formation in Lymnaea stagnalis.

The pond snail, Lymnaea stagnalis, naturally inhabits slow flowing, shallow and stagnant environments in the northern temperate zone. Consequently, it will experience wide temperature fluctuations dependent on prevailing weather conditions. We hypothesize that periods of warming act as a thermal stressor to alter memory formation. Snails were exposed to an acute 1 h period of 30°C pond water and we determined how memory formation following operant conditioning of aerial respiration was affected. In the snails used here (Dutch strain), a single 0.5 h training session (TS) results in intermediate-term (3 h) but not long-term memory (LTM). Applying the thermal stressor during training caused memory enhancement (i.e. LTM lasting 24 h). However, the breathing rate also increased in warm water, which might explain the enhanced memory. Therefore, we applied the thermal stressor (1 h at 30°C) up to 4 h before or 1 h after training. This did not alter baseline breathing rate during the period when snails would experience training. However, the thermal stressor whether experienced prior to or following the single TS, resulted in an enhanced memory that persisted up to 48h (i.e. LTM). We conclude that memory enhancement is due to the stress associated with the thermal stimulus.