Progressive Attention Guidance for Whole Slide Vulvovaginal Candidiasis Screening

Vulvovaginal candidiasis (VVC) is the most prevalent human candidal infection, estimated to afflict approximately 75% of all women at least once in their lifetime. It will lead to several symptoms including pruritus, vaginal soreness, and so on. Automatic whole slide image (WSI) classification is highly demanded, for the huge burden of disease control and prevention. However, the WSI-based computer-aided VCC screening method is still vacant due to the scarce labeled data and unique properties of candida. Candida in WSI is challenging to be captured by conventional classification models due to its distinctive elongated shape, the small proportion of their spatial distribution, and the style gap from WSIs. To make the model focus on the candida easier, we propose an attention-guided method, which can obtain a robust diagnosis classification model. Specifically, we first use a pre-trained detection model as prior instruction to initialize the classification model. Then we design a Skip Self-Attention module to refine the attention onto the fined-grained features of candida. Finally, we use a contrastive learning method to alleviate the overfitting caused by the style gap of WSIs and suppress the attention to false positive regions. Our experimental results demonstrate that our framework achieves state-of-the-art performance. Code and example data are available at https://github.com/cjdbehumble/MICCAI2023-VVC-Screening.Comment: Accepted in the main conference MICCAI 202

Characterization of Bovidae sex-determining gene SRY

In mammals, testis determination is under the control of the sex-determining gene SRY. This Y-linked gene encodes a protein with a DNA binding domain similar to those found in high-mobility-group proteins. Here we report the cloning and sequences of the SRY genes of yak and Chinese native cattle. Our data show that SRY genes in Bovidae are less divergent, especially in the coding and 3' regions

Films for optical use and methods of making such films

Films for optical use, articles containing such films, methods for making such films, and systems that utilize such films, are disclosedPublished versio

Decreased brain K(ATP) channel contributes to exacerbating ischemic brain injury and the failure of neuroprotection by sevoflurane post-conditioning in diabetic rats.

Diabetes leads to exacerbating brain injury after ischemic stroke, but the underlying mechanisms and whether therapeutic intervention with anesthetic post-conditioning can induce neuroprotection in this population are not known. We tested the hypothesis that alteration of brain mitochondrial (mito) K(ATP) channels might cause exacerbating brain injury after ischemic stroke and attenuate anesthetic post-conditioning induced neuroprotection in diabetes. We also examined whether hyperglycemic correction with insulin would restore anesthetic post-conditioning in diabetes. Non-diabetic rats and diabetic rats treated with or without insulin were subjected to focal cerebral ischemia for 2 h followed by 24 h of reperfusion. Post-conditioning was performed by exposure to sevoflurane for 15 min, immediately at the onset of reperfusion. The role of the mitoK(ATP) channel was assessed by administration of a selective blocker 5-hydroxydecanoate (5-HD) before sevoflurane post-conditioning or by diazoxide (DZX), a mitoK(ATP) channel opener, given in place of sevoflurane. Compared with non-diabetic rats, diabetic rats had larger infarct volume and worse neurological outcome at 24 h after ischemia. Sevoflurane or DZX reduced the infarct volume and improved neurological outcome in non-diabetic rats but not in diabetic rats, and the protective effects of sevoflurane in non-diabetic rats were inhibited by pretreatment with 5-HD. Molecular studies revealed that expression of Kir6.2, an important mitoK(ATP) channel component, was decreased in the brain of diabetic rats as compared to non-diabetic rats. In contrast, hyperglycemic correction with insulin in diabetic rats normalized expression of brain Kir6.2, reduced ischemic brain damage and restored neuroprotective effects of sevoflurane post-conditioning. Our findings suggest that decreased brain mitoK(ATP) channel contributes to exacerbating ischemic brain injury and the failure of neuroprotection by anesthetic post-conditioning in diabetes. Insulin glycemic control in diabetes may restore the neuroprotective effects of anesthetic post-conditioning by modulation of brain mitoK(ATP) channel