胞饮突评估子宫内膜容受性的研究进展

胚胎植入是一个复杂且受到高度调控的过程,需要囊胚与母体子宫内膜的发育精确同步。胞饮突作为表达于子宫内膜上的一种特殊膜状突起,随月经周期变化表现为不同形态,可分为发育期、成熟期及退化期。目前已有一系列研究证实,胞饮突的数量、覆盖面积及发育阶段等在预测不孕女性种植窗及评估子宫内膜容受性中具有临床价值。胞饮突评分较高、覆盖面积较广且成熟期胞饮突占比较高的女性妊娠结局更佳。其机制可能包括胞饮突通过调节宫腔内容物影响子宫内膜容受性、通过表达植入相关蛋白参与囊胚-子宫内膜相互作用等。然而,对胞饮突精准且客观的评估手段仍待进一步探索,胞饮突评估子宫内膜容受性的精确度也待进一步验证。     

The importance of genetics for timing and extent of surgery in inherited colorectal cancer syndromes

Approximately 5% of colorectal cancers arise within an inherited colorectal cancer syndrome, with known underlying genetic etiologies. These syndromes increase the risk of colorectal and extracolonic cancers. Identification of a specific genetic pathogenic variant defines the syndrome, and quantifies the elevated risks compared to the general population. Thus, knowing and understanding the risks associated with each pathogenic variant allows for risk-stratification and a more individualized management strategy. These factors influence both the timing of surgery and the extent of colorectal surgery for patients with these syndromes. Familial Adenomatous Polyposis (FAP) is a dominantly inherited polyposis syndrome caused by pathogenic variant in the APC gene and results in a near 100% chance of developing colorectal cancer if not treated. There is a genotype-phenotype correlation in which the affected gene locus is associated with severity of polyposis and the risk of desmoid disease. Prophylactic surgery ranging from total abdominal colectomy or total proctocolectomy is recommended before cancer develops. Lynch syndrome is a non-polyposis inherited syndrome caused by a pathogenic variant in MLH1, MSH2, MSH6, or PMS2. Although prophylactic colectomy in Lynch syndrome is uncommon, total abdominal colectomy as prophylaxis in the setting of colon cancer is recommended due to the likelihood of metachronous colorectal cancer. This article reviews the role of genetics surgical decision making with respect to the timing and extent of surgery within the hereditary colorectal cancer syndromes.     

进食障碍患者家庭顺应量表的汉化及信效度检验

目的 汉化进食障碍患者家庭顺应量表，并检验其信效度。方法 根据Brislin翻译模式将量表翻译成中文，通过专家函询和预调查对量表进行文化调适和修订。将量表应用于300例进食障碍患者照顾者检验信效度。结果 中文版进食障碍患者家庭顺应量表的量表水平内容效度指数为0.918。探索性因子分析结果显示5个因子可解释总变异量的49.862%。量表的各维度得分与量表总分呈中高度相关，各维度得分之间呈中低度相关或不相关。量表总Cronbach′s α为0.877，重测信度为0.883。结论 中文版进食障碍患者家庭顺应量表具有较好的信效度，可用于测量进食障碍患者的家庭顺应情况。     

The impact of sensory neuropathy and inflammation on epithelial wound healing in diabetic corneas

Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes, with several underlying pathophysiological mechanisms, some of which are still uncertain. The cornea is an avascular tissue and sensitive to hyperglycemia, resulting in several diabetic corneal complications including delayed epithelial wound healing, recurrent erosions, neuropathy, loss of sensitivity, and tear film changes. The manifestation of DPN in the cornea is referred to as diabetic neurotrophic keratopathy (DNK). Recent studies have revealed that disturbed epithelial-neural-immune cell interactions are a major cause of DNK. The epithelium is supplied by a dense network of sensory nerve endings and dendritic cell processes, and it secretes growth/neurotrophic factors and cytokines to nourish these neighboring cells. In turn, sensory nerve endings release neuropeptides to suppress inflammation and promote epithelial wound healing, while resident immune cells provide neurotrophic and growth factors to support neuronal and epithelial cells, respectively. Diabetes greatly perturbs these interdependencies, resulting in suppressed epithelial proliferation, sensory neuropathy, and a decreased density of dendritic cells. Clinically, this results in a markedly delayed wound healing and impaired sensory nerve regeneration in response to insult and injury. Current treatments for DPN and DNK largely focus on managing the severe complications of the disease. Cell-based therapies hold promise for providing more effective treatment for diabetic keratopathy and corneal ulcers.     

Total neoadjuvant therapy: Fact,fantasy, or fallacy?

Colorectal cancer is the second leading cause of cancer death in the United States for men and women, with an estimated 146,000 new cases per year - a staggering 53,000 patients die each year. Rectal cancer comprises a third of these patients, with a 5-year survival rate of 67%. Management of locally advanced rectal cancer in the U.S. had remained stagnant for more than a decade, with most of these patients being treated with long-course chemoradiotherapy, surgery, followed by adjuvant chemotherapy; adjuvant chemotherapy being administered despite lacking a high level of evidence. Over the past few years, with rectal cancer death rates exceeding 30% from metastatic disease, growing interest focused on the attributes of induction chemotherapy to eradicate minimal residual disease and purportedly increase survival. This led to the development of total neoadjuvant therapy (TNT). We now have high-quality data from randomized prospective trials to review the facts, fantasies, and fallacies of TNT.     

Anomaly segmentation in retinal images with poisson-blending data augmentation

Diabetic retinopathy (DR) is one of the most important complications of diabetes. Accurate segmentation of DR lesions is of great importance for the early diagnosis of DR. However, simultaneous segmentation of multi-type DR lesions is technically challenging because of 1) the lack of pixel-level annotations and 2) the large diversity between different types of DR lesions. In this study, first, we propose a novel Poisson-blending data augmentation (PBDA) algorithm to generate synthetic images, which can be easily utilized to expand the existing training data for lesion segmentation. We perform extensive experiments to recognize the important attributes in the PBDA algorithm. We show that position constraints are of great importance and that the synthesis density of one type of lesion has a joint influence on the segmentation of other types of lesions. Second, we propose a convolutional neural network architecture, named DSR-U-Net++ (i.e., DC-SC residual U-Net++), for the simultaneous segmentation of multi-type DR lesions. Ablation studies showed that the mean area under precision recall curve (AUPR) for all four types of lesions increased by >5% with PBDA. The proposed DSR-U-Net++ with PBDA outperformed the state-of-the-art methods by 1.7%-9.9% on the Indian Diabetic Retinopathy Image Dataset (IDRiD) and 67.3% on the e-ophtha dataset with respect to mean AUPR. The developed method would be an efficient tool to generate large-scale task-specific training data for other medical anomaly segmentation tasks.     

Inflammatory pathways in Alzheimer’s disease mediated by gut microbiota

In the past decade, numerous studies have demonstrated the close relationship between gut microbiota and the occurrence and development of Alzheimer’s disease (AD). However, the specific mechanism is still unclear. Both the neuroinflammation and systemic inflammation serve as the key hubs to accelerate the process of AD by promoting pathology and damaging neuron. What's more, the gut microbiota is also crucial for the regulation of inflammation. Therefore, this review focused on the role of gut microbiota in AD through inflammatory pathways. Firstly, this review summarized the relationship and interaction among gut microbiota, inflammation, and AD. Secondly, the direct and indirect regulatory effects of gut microbiota on AD through inflammatory pathways were described. These effects were mainly mediated by the component of the gut microbiota (lipopolysaccharides (LPS) and amyloid peptides), the metabolites of bacteria (short-chain fatty acids, branched amino acids, and neurotransmitters) and functional by-products (bile acids). In addition, potential treatments (fecal microbiota transplantation, antibiotics, probiotics, prebiotics, and dietary interventions) for AD were also discussed through these mechanisms. Finally, according to the current research status, the key problems to be solved in the future studies were proposed.