Development of the Korea-Polyenvironmental Risk Score for Psychosis

Objective Comprehensive understanding of polyenvironmental risk factors for the development of psychosis is important. Based on a review of related evidence, we developed the Korea Polyenvironmental Risk Score (K-PERS) for psychosis. We investigated whether the K-PERS can differentiate patients with schizophrenia spectrum disorders (SSDs) from healthy controls (HCs). Methods We reviewed existing tools for measuring polyenvironmental risk factors for psychosis, including the Maudsley Environmental Risk Score (ERS), polyenviromic risk score (PERS), and Psychosis Polyrisk Score (PPS). Using odds ratios and relative risks for Western studies and the “population proportion” (PP) of risk factors for Korean data, we developed the K-PERS, and compared the scores thereon between patients with SSDs and HCs. In addition, correlation was performed between the K-PERS and Positive and Negative Syndrome Scale (PANSS). Results We first constructed the “K-PERS-I,” comprising five factors based on the PPS, and then the “K-PERS-II” comprising six factors based on the ERS. The instruments accurately predicted participants’ status (case vs. control). In addition, the K-PERS-I and -II scores exhibited significant negative correlations with the negative symptom factor score of the PANSS. Conclusion The K-PERS is the first comprehensive tool developed based on PP data obtained from Korean studies that measures polyenvironmental risk factors for psychosis. Using pilot data, the K-PERS predicted patient status (SSD vs. HC). Further research is warranted to examine the relationship of K-PERS scores with clinical outcomes of psychosis and schizophrenia.     

Dynamic expression of p38beta MAPK in neurons and astrocytes after transient focal ischemia

Here we report the dynamically regulated expression of p38beta MAPK isoform in specific subsets of cells in postischemic brain. The activity of p38beta MAPK in the postischemic brain revealed biphasic induction at 30 min and 4 days after 1 h MCAO. During the early surge period, p38beta MAPK was preferentially localized in the nucleus and dendrites of neurons in the future infarction area, while during the delayed surge p38beta MAPK was heavily induced in reactive astrocytes in penumbra. The temporally and spatially regulated pattern of p38beta MAPK expression in the postischemic brain suggests distinct roles of p38beta MAPK in neuronal death and in the astrocyte activation.     

Mechanism underlying treatment of diabetic kidney disease using Traditional Chinese Medicine based on theory of Yin and Yang balance

The pathogenic mechanism of diabetic kidney disease(DKD) is complex. The development of DKD cannot be fully explained by a single mechanism.Traditional Chinese Medicine(TCM) has been applied extensively for the treatment of DKD in China.However, studying the mechanism of DKD using theories and methods that are appropriate for TCM characteristics and searching for theoretical bases for TCM clinical application are topics that still need to be explored and researched. Activation of the transforming growth factor(TGF)-β1/Smad and PI3 K/Akt/mTOR signaling pathways functions as a self-protection mechanism against renal microinflammation in DKD. However, the persistent abnormal overactivation of reactions causes secondary cell dysfunction, cell apoptosis, increased extracellular matrix(ECM) secretion, and eventually renal fibrosis. During this process, the dysregulation of self-balance among a variety of signaling pathways and the loss of self-feedback regulatory mecha-nisms downstream of these signaling pathways are critical causes of the occurrence and development of DKD. TCM may both inhibit the expression or activation of hyperactive signaling pathways(NFB, Smad3, and PI3 K/Akt/mTOR) and increase the expression or activation of deficient signaling pathways(Smad7 and PTEN) to restore balance to cells with an abnormal pathophysiological status and achieve the goal of DKD treatment.     

Takotsubo cardiomyopathy： A case report

Takotsubo cardiomyopathy （TC） is a reversible non-ischemic cardiomyopathy characterized by transient left ventricular dysfunction, which is usually associated with a favorable prognosis. It is similar to an acute myocardial infarction, but coronary angiography shows no obstructive lesions and akinesia of the apex and the middle portion of the left ventricle. TC is often triggered by an intense physical or emotional stress event. Without appreciation of differentiating features, TC can easily be misdiagnosed as an acute coronary syndrome. Misdiagnosis and the subsequent inappropriate and potentially harmful use of medication therapy can be avoided through detailed history-taking, laboratory examination and proper investigations. In order to raise the awareness of the importance of TC diagnosis and further to discuss the therapeutic strategies, we are going to present a case report regarding TC and provide a timely summary and update on current understand- ing.     

TLR2 as an essential molecule for protective immunity against Toxoplasma gondii infection

To investigate the role of the Toll-like receptor (TLR) family in host defense against Toxoplasma gondii, we infected TLR2-, TLR4- and MyD88-deficient mice with the avirulent cyst-forming Fukaya strain of T. gondii. All TLR2- and MyD88-deficient mice died within 8 days, whereas all TLR4-deficient and wild-type mice survived after i.p. infection with a high dose of T. gondii. Peritoneal macrophages from T. gondii-infected TLR2- and MyD88-deficient mice did not produce any detectable levels of NO. T. gondii loads in the brain tissues of TLR2- and MyD88-deficient mice were higher than in those of TLR4-deficient and wild-type mice. Furthermore, high levels of IFN-gamma and IL-12 were produced in peritoneal exudate cells (PEC) of TLR4-deficient and wild-type mice after infection, but low levels of cytokines were produced in PEC of TLR2- and MyD88-deficient mice. On the other hand, high levels of IL-4 and IL-10 were produced in PEC of TLR2- and MyD88-deficient mice after infection, but low levels of cytokines were produced in PEC of TLR4-deficient and wild-type mice. The most remarkable histological changes with infiltration of inflammatory cells were observed in lungs of TLR2-deficient mice infected with T. gondii, where severe interstitial pneumonia occurred and abundant T. gondii were found.     

利用表面肌电信号评价肌肉疲劳的方法

表面肌电信号分析是评价局部肌肉疲劳有效的工具。过去由于受信号处理技术的限制,对肌肉疲劳的评价仅局限于等长、恒力收缩。由于适合于非平稳信号分析的频谱估计技术的发展,使得动态收缩条件下的肌肉疲劳评价得以实现,在工效学、康复医学和运动医学等方面开启了新的应用领域。本文论述了利用表面肌电信号评价肌肉疲劳,特别是在肌肉动态收缩期间评价肌肉疲劳的方法,为进一步探讨肌肉疲劳的发生机制提供理论依据。     

犬牙槽骨牵张成骨的生物力学和组织学分析

背景：牙槽骨牵张成骨是解决严重牙槽骨萎缩的重要方法,其成骨过程和生物力学对于以后的种植和修复极为重要,目前一直缺少相关的实验研究。 目的：分析犬牙槽骨牵张成骨的生物力学和组织学特点。 方法：先拔除12只杂种犬双侧下颌前磨牙,牙槽骨修整后,制作萎缩牙槽骨模型。3个月后,植入骨内型牙槽骨牵张器。经过7 d的间歇期,以1 mm/d,1次/d的频率进行牙槽骨垂直向增高。在固定期的1,2和3个月,对牵张后的牙槽骨进行临床、生物力学、放射学和组织学检测。 结果与结论：所有牵张器与周围组织愈合良好。牵张结束时,临床和放射学检查显示：萎缩牙槽骨分别增高 (4.80±0.50) mm和(5.12±0.67) mm。组织学检测发现牵张区骨小梁在固定期的1-3个月成熟,其剪切力逐步提高,固定期3个月时和自体骨的剪切力相当。结果显示牙槽骨牵张成骨的组织学和生物力学性能在固定期3个月时与自体骨相当。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

基于电刺激的外层型人工视网膜的研究进展

外层型视网膜假体采用了MEMS技术,通过植入到视网膜相应部位的电极来刺激神经节细胞,并且能够在大脑皮层视觉区域引起对应的特征电位反应,最终部分恢复生物体的视觉.这种外层型视网膜植入装置可分为眼外和眼内部分.后者功能相对重要,设计也较为复杂.它是由包含MPDA和微电极的刺激芯片及附属装置组成.本篇文章主体包括四部分:首先是视网膜假体的概况;其次是视网膜生理基础和视网膜假体理论的简介;在第三部分,为设计理念和MPDA的制造过程;最后,是对难题的讨论和未来发展的展望.     

Nickel release behavior and surface characteristics of porous NiTi shape memory alloy modified by different chemical processes

As a non-line-of-sight surface modification technique, chemical treatment is an effective method to treat porous NiTi with complex surface morphologies and large exposed areas due to its liquidity and low temperature. In the work described here, three different chemical processes are used to treat porous NiTi alloys. Our results show that H(2)O(2) treatment, NaOH treatment, and H(2)O(2) pre-treatment plus subsequent NaOH treatment can mitigate leaching of nickel from the alloy. The porous NiTi samples modified by the two latter processes favor deposition of a layer composed of Ca and P due to the formation of bioactive Na(2)TiO(3) on the surface. Among the three processes, H(2)O(2) pre-treatment plus subsequent NaOH modification is the most effective in suppressing nickel release. Small area X-ray photoelectron spectroscopy reveals that the surfaces treated by different chemical processes have different structures and compositions. The sample modified by the H(2)O(2) treatment is composed of rough TiO(2) on the outer surface and an oxide transition layer underneath whereas the sample treated by NaOH comprises a surface layer of titanium oxide and Na(2)TiO(3) together with a transition layer. The sample processed by the H(2)O(2) and NaOH treatment has a pure Na(2)TiO(3) layer on the surface and a transition layer underneath. These results help to elucidate the different nickel release behavior and bioactivity of porous NiTi alloys processed by different methods.