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The slow loris (Genus Nycticebus) is a group of small, nocturnal and venomous primates with a distinctive locomotion mode. The detection of slow loris plays an important role in the subsequent individual identification and behavioral recognition and thus contributes to formulating targeted conservation strategies, particularly in reintroduction and post-release monitoring. However, fewer studies have been conducted on efficient and accurate detection methods of this endangered taxa. The traditional methods to detect the slow loris involve long-term observation or watching surveillance video repeatedly, which would involve manpower and be time consuming. Because humans cannot maintain a high degree of attention for a long time, they are also prone to making missed detections or false detections. Due to these observational challenges, using computer vision to detect slow loris presence and activity is desirable. This article establishes a novel target detection dataset based on monitoring videos of captive Bengal slow loris (N. bengalensis) from the wildlife rescue centers in Xishuangbanna and Pu’er, Yunnan, China. The dataset is used to test two improvement schemes based on the YOLOv5 network: (1) YOLOv5-CBAM + TC, the attention mechanism and deconvolution are introduced; (2) YOLOv5-SD, the small object detection layer is added. The results demonstrate that the YOLOv5-CBAM + TC effectively improves the detection effect. At the cost of increasing the model size by 0.6 MB, the precision rate, the recall rate and the mean average precision (mAP) are increased by 2.9%, 3.7% and 3.5%, respectively. The YOLOv5-CBAM + TC model can be used as an effective method to detect individual slow loris in a captive environment, which helps to realize slow loris face and posture recognition based on computer vision.

(1) Background: The aim of this longitudinal study was to evaluate the association between disease progression according to the Milano–Torino staging (MITOS) system and long-term survival in Chinese patients with amyotrophic lateral sclerosis (ALS). We also examined factors affecting MITOS progression. (2) Methods: Patients were enrolled and underwent follow-up at 6, 12, 18, and 24 months, and their demographic and clinical data, including the Milano–Torino stage, Amyotrophic Lateral Sclerosis Functional Rating Scale—Revised (ALSFRS-R) score and neuropsychiatric data, were evaluated. The sensitivity and specificity of predicting survival outcomes based on MITOS progression and ALSFRS-R score decline from baseline to 6 months were compared. The associations between MITOS progression from baseline to 6 months and survival outcome at 12, 18 and 24 months were examined, and factors associated with disease progression were evaluated with subgroup analyses. (3) Results: Among the 100 patients included, 74% were in stage 0 at baseline, and approximately 95% progressed to a higher stage of the MITOS system at 24 months. MITOS progression from baseline to 6 months and ALSFRS-R decline showed comparable value for predicting survival at 12, 18, and 24 months. MITOS progression from baseline to 6 months is strongly associated with death outcomes. Older age at onset and increased depression and anxiety scores may be related to disease progression. (4) Conclusions: MITOS progression during the early disease course could serve as a prognostic marker of long-term survival and may have utility in clinical trials. Age at onset and diagnosis and neuropsychiatric factors might be associated with disease progression.

Ischemic stroke, characterized by the disturbance of the blood supply to the brain, is a severe worldwide health threat with high mortality and morbidity. However, there is no effective pharmacotherapy for ischemic injury. Currently, combined treatment is highly recommended for this devastating injury. In the present study, we investigated neuroprotective effects of the combination of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) and Lyciumbarbarum polysaccharide (LBP) on cortical neurons using an in vitro ischemic model. Our study demonstrated that treatment with docosahexaenoic acid (DHA), a major component of the ω-3 PUFAs family, significantly inhibited the increase of intracellular Ca2+ in cultured wild type (WT) cortical neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R) injury and promoted their survival compared with the vehicle-treated control. The protective effects were further confirmed in cultured neurons with high endogenous ω-3 PUFAs that were isolated from fat-1 mice, in that a higher survival rate was found in fat-1 neurons compared with wild-type neurons after OGD/R injury. Our study also found that treatment with LBP (50 mg/L) activated Trk-B signaling in cortical neurons and significantly attenuated OGD/R-induced cell apoptosis compared with the control. Notably, both combining LBP treatment with ω-3 PUFAs administration to WT neurons and adding LBP to fat-1 neurons showed enhanced effects on protecting cortical neurons against OGD/R injury via concurrently regulating the intracellular calcium overload and neurotrophic pathway. The results of the study suggest that ω-3 PUFAs and LBP are promising candidates for combined pharmacotherapy for ischemic stroke.