Background: Widespread early dementia detection could drastically increase clinical trial candidates and enable early interventions. Since the Clock Drawing Test (CDT) can be potentially used for diagnosing dementia related diseases, it can be leveraged to devise a computer-aided screening tool. Objective: This work aims to develop an online screening tool by leveraging Artificial Intelligence and the CDT. Methods: Images of an analog clock drawn by 3,263 cognitively intact and 160 impaired subjects were used. First, we processed the images from the CDT by a deep learning algorithm to obtain dementia scores. Then, individuals were classified as belonging to either category by combining CDT image scores with the participants age. Results: We have evaluated the performance of the developed models by applying 5-fold cross validation on 20% of the dataset. The deep learning model generates dementia scores for the CDT images with an Area Under the ROC Curve (AUC) of 81.3%. A composite logistic regression model using age and the generated dementia scores, yielded an average AUC and average weighted F1 score of 92% and 94.4% , respectively. Discussion: CDT images were subjected to distortion consistent with an image drawn on paper and photographed by a cell phone. The model offers a cost-effective and easily deployable mechanism for detecting cognitive impairment online, without the need to visit a clinic.

Human tumors are frequently infiltrated by numerous monocytes/macrophages, which can be found within the tumor mass (intratumoral) or surrounding the tumor (peritumoral). The functional role that these monocytes/macrophages play in tumor growth is controversial. To address this issue we inhibited intratumoral monocyte/macrophage recruitment with mAbs that either blocked integrin function or neutralized a tumor-produced chemotactic protein. Both treatments significantly increased tumor formation and accelerated tumor growth. Surprisingly, the same results were obtained when recruitment of peritumoral or intratumoral monocytes/macrophages was blocked. Our findings are contrary to one of the purported roles of monocytes/macrophages, particularly in the peritumoral area, since we found no evidence for monocyte/macrophage-supported tumor growth. These results provide direct evidence that intratumoral as well as peritumoral monocytes/macrophages act to limit tumor size in the early stages following tumor inoculation and provide a mechanism that accounts for monocyte/macrophage recruitment to human tumors.

Purpose: To apply a novel visible and near-infrared optical coherence tomography (vnOCT) in the dexamethasone-induced ocular hypertension mouse model, and test the capability of four optical markers, peripapillary retinal nerve fiber layer (RNFL) thickness, total retinal blood flow, VN ratio and hemoglobin oxygen saturation (sO2), in detecting retinal ganglion cell (RGC) damage in association with ocular hypertension.Methods: Twelve mice (C57BL/6J) were separated into a control (n=6) and a dexamethasone group (n=6) receiving twice daily saline or dexamethasone eye drops, respectively, for 7 weeks. Intraocular pressure (IOP) measurements were taken at baseline and weekly. Optical measurements by vnOCT were longitudinally taken at baseline, 4 weeks and 7 weeks. Following week 7, ex vivo RGC counting was performed by immunostaining. Results:The dexamethasone group showed a measurable rise in IOP by week 2. Despite the IOP differences between the dexamethasone and control groups, there was not a statistical difference in RNFL thickness or total blood flow over 7 weeks. The dexamethasone group did show an increase in retinal arteriovenous sO2 difference (A-V sO2) that was significant at week 4 and 7. The RNFL VN ratio showed a significant decrease at week 4 and 7 in dexamethasone group associated with a decreased RGC count.Conclusions: RNFL VN ratio and A-V sO2 are capable of detecting early retinal alterations in the dexamethasone-induced ocular hypertension mouse model. Data analysis suggests VN ratio and A-V sO2 are correlated with RGC loss secondary to ocular hypertension, while being independent of IOP.