Abstract:Mitochondrial ultrastructure is a fine structure observed by electron microscope, which can be changed according to different energy requirements and physiological environment, and plays a key role in regulating mitochondrial function. The structure of mitochondrial cristae is an important mitochondrial ultrastructure, which affects many mitochondrial diseases. Therefore, studying the function and understanding the regulation mechanism of mitochondrial ultrastructure have important guiding significance for studying mitochondrial diseases and looking for therapeutic targets. This paper introduces the main regulating mechanism of mitochondrial cristae in detail, and focuses on the research progress in the composition of mitochondrial ultrastructure, the effect of mitochondrial ultrastructure on mitochondrial function, and the relationship between mitochondrial ultrastructure and mitochondrial disease, in order to provide theoretical reference for developing more effective mitochondrial disease treatment.

Abstract:Aging is an emerging and important research area. With the accumulation of knowledge in related fields and the advancement of technology, people gradually realized that aging itself can be intervened and it is of great scientific and practical significance to delay aging, especially delaying the occurrence and development of age-related diseases. Among the many factors that cause individual aging, the accumulation of senescent cells is considered to be an important reason that leads to organ aging and degeneration, and finally causes the age-related diseases. In recent years, a number of studies have shown that removing senescent cells in vivo can delay the occurrence of multiple age-related diseases, which directly proves that senescent cells are one of the important causes of age-related diseases, providing a new target for the treatment of age-related diseases. Cellular senescence is generally considered due to the activation of cell cycle inhibition pathway induced by accumulation of damages, and the cells permanently exit the proliferation cycle. Senescent cells undergo changes in cell morphology, transcriptional profiles, protein homeostasis, epigenome and metabolism. Moreover, senescent cells resist apoptosis and therefore accumulate in multiple organs and tissues in the body. Senescent cells secrete a number of inflammatory factors, leading to a local non-infectious inflammatory tissue microenvironment, which will cause organ function deterioration and a variety of age-related diseases. Therefore, several research groups have screened the library of small molecular compounds and found that certain compounds can selectively eliminate senescent cells by targeting pathways underpinning senescent cells" resistance to apoptosis. These small molecular compounds are called " senolytics ", denoting compounds for killing senescent cells. Senolytics have been shown to alleviate multiple age-related diseases and prolong the lifespan in animal models. Therefore, targeted killing of senescent cells has an important clinical application prospect for the treatment of a variety of age-related diseases so as to improve the healthy lifespan. In addition, strategies such as stem cell transplantation, gene editing and heterochronic parabiosis are also of great significance and inspiration in the development of anti-aging research. By summarizing the recent important progress in the field of senescent cell clearance and a variety of anti-aging strategies, this paper briefly reviews the history of cellular senescence research, discusses the relationship between cellular senescence and age-related diseases, emphasizing on the potential therapeutic applications by targeting senescent cells and the limitations, as well as the further research directions in this field.

Abstract:Cell/bacteria-driven drug-delivery systems have been demonstrated as a promising drug delivery strategy. This strategy majors on kinds of inherent biocarriers combined with medicine, and effectively overcomes the shortcomings of classical nano-drug in bioavailability, targeting ability and tissue penetration. Benefitted from the specific response to the target lesion, these systems could not only achieve efficient and active targeting drug delivery, but also reduced the toxic and side effects on normal tissues. At present, these biocarriers have been widely applied in drug delivery, showing broad application prospects in the fields of accurate disease diagnosis and treatment. Here, we have reviewed the research and explore the development trend of cell/bacteria-driven drug-delivery systems.

Abstract:Reperfusion after acute myocardial infarction is the only way to rescue ischemic myocardium, but recovery of blood flow may lead to ischemia/reperfusion (I/R) injury. Long non-coding RNA (lncRNA) and pyroptosis are involved in the pathological process of myocardial I/R injury and play important roles in it. LncRNA can directly or indirectly act on pyroptosis signaling pathway related proteins, and then regulate various pathological processes including myocardial I/R injury. In this review the roles of lncRNA and pyroptosis in myocardial I/R are summarized to further explore the relationship between them and provide new ideas for the prevention and treatment of myocardial I/R injury.

Abstract:Mitochondrial-mediated apoptosis plays an important role for chemotherapeutic drugs in inducing cancer cell death,which also helps maintain homeostasis of the internal environment in normal organisms. In cancer cells, the dysregulation of apoptosis becomes a barrier for cancer cells to escape from the killing effect of chemotherapeutic drugs. In regulating mitochondrial-induced apoptosis, BCL-2 family proteins are of great importance. Therefore, a detection technology based on BCL-2 family proteins, BH3-profiling technology emerged. The proposed technology may provide new ideas for the personalized treatment of cancer. This paper focuses on the principle of BH3-profiling technology, its application in the selection of cancer chemotherapeutic drugs and the development of new chemotherapeutic drugs.

Abstract:C-type lectins (CTLs) are a family of carbohydrate-binding proteins that share a common structural motif; they are quite conserved evolutionarily from arthropods to mammals and play an essential role in immune responses. Aedes aegypti is a pivotal vector for the dengue virus and expresses more than 30 types of C-type lectins, which are critical for both viral and bacterial infections. A recent study indicates that mosGCTL-3 interacts with a dengue virus-2 envelope protein (DENV-2 E protein) in vivo and in vitro thereby enhancing the infection of A. aegypti. Here, in this report we found another C-type lectin protein, mosGCTL-2 with important functions similar to mosGCTL-3. Results from the phylogenetic tree analysis suggested that there is sequence similarity between mosGCTL-2 and mosGCTL-3, with 43.56% of their amino acid sequences being identical. We constructed Drosophila S2 cell expression system to purify mosGCTL-2. In vitro experiments showed that mosGCTL-2 binds to the DENV-2 E protein through a calcium-dependent manner. The upregulation of mosGCTL-2 was noted in A. aegypti and was important for dengue virus 2 (DENV-2) infection in vivo. These findings suggest that mosGCTL-2 may be a pattern recognition receptor that performs an important function in the infection of A. aegypti by the dengue virus.

Abstract:The detection of diseased cells in blood is an important method in cancer diagnosis and treatment. The existence of cancerous cells in the blood indicates that the body have been already canceration. Therefore, the identification and detection of the cancerous cells has the significant meaning in the medical science. Polarization is an inherent characteristic of light. The properties of different substances can be detected by their different polarization characteristics of light. In this article，we discussed the property of the cancerous cells firstly used the polarized light scattering method. Base on the different character in polarized light, we successfully distinguished the cancerous cells and erythrocyte, the viable cancerous cell and the dead cancerous cell. This method is non-invasive, non-in, high-sensitive and high-resolution compared to other ones. It provide the new ideas for cancer diagnosis and treatment.

Abstract:RNA editing is an important post-transcriptional modification process. There are many algorithms used to identify RNA editing. This study of the sequencing depth’s effect on RNA editing will provide a suggested method for RNA editing research. Mouse reference genome was mapped to the RNA-seq by STAR. Then identified SNV by GATK, finally RNA Editing sites were filtered by Separate method, GIREMI and RNAEditor. The results showed the identification of RNA editing varied in three methods. There was little overlap in results. As the sequencing depth increases, the identified number of RNA editing sites also increases. In conclusion, the identification of RNA editing sites is positive correlated with the sequencing depth.

Abstract:Breast cancer is one of the most common malignant tumors in women, aromatase inhibitors (AIs) are an important adjuvant therapy of breast cancer. Formestane (4-OHA), one of steroidal AIs, is used to treat advanced breast cancer and inhibits irreversibly aromatase activity. Several previous studies have found that aldo-keto reductases AKR1Cs are involved in the metabolism of many steroids and their derivatives. In the future they may be targets of therapy of hormonal diseases. We presumed that AKR1Cs may participate in site-specific metabolism of 4-OHA, affecting its therapeutic effect. In this paper, four active AKR1C isoforms were obtained by prokaryotic expression in vitro. The catalytic efficiency of AKR1Cs was detected by spectroscopic methods, and the effect of inhibitors on the catalytic reduction of 4-OHA by AKR1Cs was verified. It was found that four AKR1C isoforms can reduce keto-groups and double bonds of 4-OHA. AKR1C4 can rapidly catalyze the structural changes in 4-OHA with a conversion rate of almost 100%, followed by AKR1C3 and AKR1C1 with a conversion efficiency of about 30%. AKR1C2 has the lowest activity towards of 4-OHA, and the conversion efficiency is only about 20%. At the same time, the inhibitor showed a significant dose-effect relationship with AKR1Cs. Non-linear regression analysis showed that the inhibitors had a strong affinity for AKR1C3 and AKR1C4 with IC₅₀ values of 47.4 μmol/L and 54.68 μmol/L, respectively. The inhibition of AKR1C1 and AKR1C2 is relatively weak, and the IC₅₀ values are 77.37 μmol/L and 82.24 μmol/L, respectively. The above results indicate that 4-OHA can be rapidly metabolized by AKR1C4 which is expressed in the liver only which may contribute to the fact that 4-OHA and its many conjugated metabolites is not very effective after oral administration. Our data support the advantage of parenteral administration of the drug as a depot-formulation or as a preparation for transdermal delivery and also provides a new idea for further research on nano-drug carriers and derivatives of the drug in the future.