浅谈口腔医学硕士研究生科研作图能力的培养

科研作图是展示研究数据的主要形式,也是科研素养的重要体现。口腔医学硕士研究生是接触科学研究的第一站,然而目前的研究生教育环节对科研作图能力缺乏系统性培养,许多研究生在科研作图中存在许多不规范的问题,本文针对这一问题进行初步探讨。本文分析比较了常用作图工具Microsoft Excel、Origin和Graphpad Prism的特点;以学校口腔医学硕士的培养过程为参考,分析目前硕士研究生科研作图方面存在的主要问题及应对策略。发现不同作图软件具有不同的风格特点,当前硕士研究生作图存在风格不统一、拼图不规范、图注不规范等问题,应当根据自身需求合理选择作图工具,提升作图能力。科研作图是科研能力的重要方面,应当加强口腔医学硕士研究生作图能力的培养。     

基于家庭的心理治疗对强迫障碍治疗的研究进展

强迫障碍(obsessive-compulsive disorder,OCD)是常见的难治性精神疾病,经过心理治疗和药物治疗仅有40%~60%患者获得缓解,患者残留各种症状和功能障碍。心理治疗是OCD治疗的重要组成部分,家庭因素在疾病的发生、维持和预后中起重要作用,以家庭为基础的心理治疗越来越受到重视。文章就对OCD采用基于家庭的心理治疗的必要性和进展进行综述,研究显示患者家属的精神心理状态和家庭顺应性等因素与OCD治疗效果密切相关,而家庭成员高度参与,针对家庭因素干预的基于家庭的心理治疗策略可以增强治疗效果,改善患者家庭功能。文章为强迫障碍的临床优化治疗提供了实践依据。     

Neutrophil proteases degrade autoepitopes of NET-associated proteins

Neutrophils can form neutrophil extracellular traps (NETs) to capture microbes and facilitate their clearance. NETs consist of decondensed chromatin decorated with anti-microbial proteins. Here, we describe the effect of neutrophil proteases on the protein content of NETs. We show that the neutrophil serine proteases degrade several neutrophil proteins associated with NETs. Interestingly, the anti-bacterial proteins associated with NETs, such as myeloperoxidase, calgranulin B and neutrophil elastase (NE), seem to be less susceptible to proteolytic degradation than other NET proteins, such as actin and MNDA. NETs have been proposed to play a role in autoimmune reactions. Our data demonstrate that a large number of the autoepitopes of NET proteins that are recognized by autoantibodies produced by systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients are also removed by the proteases. In conclusion, neutrophil serine proteases have a major impact on the NET proteome and the proteolytic changes of NET-associated proteins may counteract autoimmune reactions to NET components.     

Epithelial ovarian cancer risk: A review of the current genetic landscape

Ovarian cancer is the fourth most common cause of cancer-related death in women in the developed world, and one of the most heritable cancers. One of the most significant risk factors for epithelial ovarian cancer (EOC) is a family history of breast and/or ovarian cancer. Combined risk factors can be used in models to stratify risk of EOC, and aid in decisions regarding risk-reduction strategies. Germline pathogenic variants in EOC susceptibility genes including those involved in homologous recombination and mismatch repair pathways are present in approximately 22% to 25% of EOC. These genes are associated with an estimated lifetime risk of EOC of 13% to 60% for BRCA1 variants and 10% to 25% for BRCA2 variants, with lower risks associated with remaining genes. Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) thought to explain an additional 6.4% of the familial risk of ovarian cancer, with 34 susceptibility loci identified to date. However, an unknown proportion of the genetic component of EOC risk remains unexplained. This review comprises an overview of individual genes and SNPs suspected to contribute to risk of EOC, and discusses use of a polygenic risk score to predict individual cancer risk more accurately.     

Embryonic skull development in the gecko,Tarentola annularis (Squamata: Gekkota: Phyllodactylidae)

Tarentola annularis is a climbing gecko with a wide distribution in Africa north of the equator. In the present paper, we describe the development of the osteocranium of this lizard, from the first appearance of the cranial elements up to the point of hatching. This is based on a combination of histology and cleared and stained specimens. This is the first comprehensive account of gekkotan pre-hatching skull development based on a comprehensive series of embryos, rather than a few selected stages. Given that Gekkota is now widely regarded as representing the sister group to other squamates, this account helps to fill a significant gap in the literature. Moreover, as many authors have considered features of the gekkotan skull and skeleton to be indicative of paedomorphosis, it is important to know whether this hypothesis is supported by delays in the onset of cranial ossification. In fact, we found the sequence of cranial bone ossification to be broadly comparable to that of other squamates studied to date, with no significant lags in development.     

2009-2019年西安市肺结核流行特征及治疗转归分析

目的 了解2009-2019年西安市肺结核的流行特征及治疗转归情况，为完善西安市肺结核防治策略提供依据。方法 收集2009-2019年《传染病信息管理系统》中登记的肺结核患者病案信息数据，通过描述性研究方法对肺结核流行病学特征和治疗转归情况进行分析。结果 2009-2019年间西安市肺结核年平均发病率为49.06/10万。郊县、郊区、城区肺结核年平均发病率分别为54.13/10万、47.46/10万和46.19/10万；男性发病率是女性的1.85倍。职业分布排在前5位的为农民（47.48%），家政、家务及待业（14.65%），离退人员（9.55%），学生（8.63%）和工人（5.23%）。利福平敏感或耐药性未知患者的成功治疗率平均为98.03%，利福平耐药患者治疗成功率为51.47%。结论 西安市近年来肺结核发病率和治疗率呈增长趋势，利福平耐药患者治疗成功率较低，要加强对重点人群的健康促进工作，加大肺结核发现力度及患者治疗管理工作。     

Biomarkers on patient T cells diagnose active tuberculosis and monitor treatment response

BACKGROUND. The identification and treatment of individuals with tuberculosis (TB) is a global public health priority. Accurate diagnosis of pulmonary active TB (ATB) disease remains challenging and relies on extensive medical evaluation and detection of Mycobacterium tuberculosis (Mtb) in the patient’s sputum. Further, the response to treatment is monitored by sputum culture conversion, which takes several weeks for results. Here, we sought to identify blood-based host biomarkers associated with ATB and hypothesized that immune activation markers on Mtb-specific CD4⁺ T cells would be associated with Mtb load in vivo and could thus provide a gauge of Mtb infection.METHODS. Using polychromatic flow cytometry, we evaluated the expression of immune activation markers on Mtb-specific CD4⁺ T cells from individuals with asymptomatic latent Mtb infection (LTBI) and ATB as well as from ATB patients undergoing anti-TB treatment.RESULTS. Frequencies of Mtb-specific IFN-γ⁺CD4⁺ T cells that expressed immune activation markers CD38 and HLA-DR as well as intracellular proliferation marker Ki-67 were substantially higher in subjects with ATB compared with those with LTBI. These markers accurately classified ATB and LTBI status, with cutoff values of 18%, 60%, and 5% for CD38⁺IFN-γ⁺, HLA-DR⁺IFN-γ⁺, and Ki-67⁺IFN-γ⁺, respectively, with 100% specificity and greater than 96% sensitivity. These markers also distinguished individuals with untreated ATB from those who had successfully completed anti-TB treatment and correlated with decreasing mycobacterial loads during treatment.CONCLUSION. We have identified host blood-based biomarkers on Mtb-specific CD4⁺ T cells that discriminate between ATB and LTBI and provide a set of tools for monitoring treatment response and cure.TRIAL REGISTRATION. Registration is not required for observational studies.FUNDING. This study was funded by Emory University, the NIH, and the Yerkes National Primate Center.     

Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models

Microglia, the innate immune cells of the CNS, perform critical inflammatory and noninflammatory functions that maintain normal neural function. For example, microglia clear misfolded proteins, elaborate trophic factors, and regulate and terminate toxic inflammation. In Alzheimer’s disease (AD), however, beneficial microglial functions become impaired, accelerating synaptic and neuronal loss. Better understanding of the molecular mechanisms that contribute to microglial dysfunction is an important objective for identifying potential strategies to delay progression to AD. The inflammatory cyclooxygenase/prostaglandin E2 (COX/PGE₂) pathway has been implicated in preclinical AD development, both in human epidemiology studies and in transgenic rodent models of AD. Here, we evaluated murine models that recapitulate microglial responses to Aβ peptides and determined that microglia-specific deletion of the gene encoding the PGE₂ receptor EP2 restores microglial chemotaxis and Aβ clearance, suppresses toxic inflammation, increases cytoprotective insulin-like growth factor 1 (IGF1) signaling, and prevents synaptic injury and memory deficits. Our findings indicate that EP2 signaling suppresses beneficial microglia functions that falter during AD development and suggest that inhibition of the COX/PGE₂/EP2 immune pathway has potential as a strategy to restore healthy microglial function and prevent progression to AD.