Cooperation, innovation and transition： the new focus of the China Interventional Therapeutics （CIT） congress

Since its inauguration in 2003, China Interventional Therapeutics （CIT） congress has witnessed the growth of percutaneous cardiovascular intervention in China. In 2003 the total number ofpercutaneous coronary intervention （PCI） in China was about 40 000 cases,1 while by CIT＇s 10th anniversary in 2012, the annual number of PCI in China had reached 340 000 cases. CIT has grown along with PCI practice in the country; last year the CIT congress hosted 6000 attendees, including 180 international faculty members and over 750 foreign participants from 42 countries or regions.

Crosslink between mutations in mitochondrial genes and brain disorders:implications for mitochondrial-targeted therapeutic interventions

At the present,association of mitochondrial dysfunction and progression of neurological disorders has gained significant attention.Defects in mitochondrial network dynamics,point mutations,deletions,and interaction of pathogenomic proteins with mitochondria are some of the possible underlying mechanisms involved in these neurological disorders.Mitochondrial genetics,defects in mitochondrial oxidative phosphorylation machinery,and reactive oxygen species production might share common crosstalk in the progression of these neurological disorders.It is of significant interests to explore and develop therapeutic strategies aimed at correcting mitochondrial abnormalities.This review provided insights on mitochondrial dysfunction/mutations involved in the progression of Alzheimer’s disease,Huntington’s disease,and epilepsy with a special focus on Parkinson’s disease pathology.Along with the deleterious effects of mitochondrial mutations in aforesaid neurological disorders,this paper unraveled the available therapeutic strategy,specifically aiming to improve mitochondrial dysfunction,drugs targeting mitochondrial proteins,gene therapies aimed at correcting mutant mtDNA,peptide-based approaches,and lipophilic cations.

Mitochondria in Huntington’s disease:implications in pathogenesis and mitochondrial-targeted therapeutic strategies

Huntington’s disease is a genetic disease caused by expanded CAG repeats on exon 1 of the huntingtin gene located on chromosome 4.Compelling evidence implicates impaired mitochondrial energetics,altered mitochondrial biogenesis and quality control,disturbed mitochondrial trafficking,oxidative stress and mitochondrial calcium dyshomeostasis in the pathogenesis of the disorder.Unfortunately,conventional mitochondrial-targeted molecules,such as cysteamine,creatine,coenzyme Q10,or triheptanoin,yielded negative or inconclusive results.However,future therapeutic strategies,aiming to restore mitochondrial biogenesis,improving the fission/fusion balance,and improving mitochondrial trafficking,could prove useful tools in improving the phenotype of Huntington’s disease and,used in combination with genome-editing methods,could lead to a cure for the disease.

Long noncoding RNA LINC02568 sequesters microRNA-874-3p to facilitate malignancy in breast cancer cells via cyclin E1 overexpression

Increasing numbers of long noncoding RNAs(lncRNAs)are implicated in breast cancer oncogenicity.However,the contribution of LINC02568 toward breast cancer progression remains unclear and requires further investigation.Herein,we evaluated LINC02568 expression in breast cancer and clarified its effect on disease malignancy.We also investigated the mechanisms underlying the pro-oncogenic role of LINC02568.Consequently,LINC02568 was upregulated in breast cancer samples,with a notable association with worse overall survival.Functionally,depleted LINC02568 suppressed cell proliferation,colony formation,and metastasis,whereas LINC02568 overexpression exerted the opposite effects.Our mechanistic investigations suggested that LINC02568 was physically bound to and sequestered microRNA-874-3p(miR-874-3p).Furthermore,miR-874-3p mediated suppressive effects in breast cancer cells by targeting cyclin E1(CCNE1).LINC02568 positively controlled CCNE1 expression by sequestering miR-874-3p.Rescue experiments revealed that increased miR-874-3p or decreased CCNE1 expression recovered cell growth and motility functions induced by LINC02568 in breast cancer cells.In conclusion,the tumor-promoting functions of LINC02568 in breast cancer cells were enhanced by sequestering miR-874-3p and consequently over-expressing CCNE1.Our data may facilitate the identification of novel therapeutic targets in clinical settings.

Potential therapeutic interventions based on the role of the endoplasmic reticulum stress response in progressive neurodegenerative diseases

In 1945,Porter et al.published an electon microscopy study of cultured chick fibroblasts in which they observed：＇a granular background and details of a darker lacelike reticulum which in places appears to be made up of chains of＂vesicles＂＇（Porter et al.,1945）.This constituted the first published observation of the endoplasmic reticulum（ER）and,while it was not evident at that time,this cytoplasmic system of interconnecting membrane-lined channels, comprising vesicles, tubules and cisternae, has numerous important functions.

Human Ebola virus infection in West Africa: a review of available therapeutic agents that target different steps of the life cycle of Ebola virus

The recent outbreak of the human Zaire ebolavirus(EBOV)epidemic is spiraling out of control in West Africa.Human EBOV hemorrhagic fever has a case fatality rate of up to 90%.The EBOV is classified as a biosafety level 4 pathogen and is considered a category A agent of bioterrorism by Centers for Disease Control and Prevention,with no approved therapies and vaccines available for its treatment apart from supportive care.Although several promising therapeutic agents and vaccines against EBOV are undergoing the Phase I human trial,the current epidemic might be outpacing the speed at which drugs and vaccines can be produced.Like all viruses,the EBOV largely relies on host cell factors and physiological processes for its entry,replication,and egress.We have reviewed currently available therapeutic agents that have been shown to be effective in suppressing the proliferation of the EBOV in cell cultures or animal studies.Most of the therapeutic agents in this review are directed against non-mutable targets of the host,which is independent of viral mutation.These medications are approved by the Food and Drug Administration(FDA)for the treatment of other diseases.They are available and stockpileable for immediate use.They may also have a complementary role to those therapeutic agents under development that are directed against the mutable targets of the EBOV.

Microbiome meets microglia in neuroinflammation and neurological disorders

One of the emerging hot topics in biosciences is the intriguing link between gut microbial communities and its influences outside the gastrointestinal tract, such as the central nervous system (CNS), including its cognitive activities and immune responses. Beyond its neuroprotective properties, microglia are also critical for neuronal synaptic pruning and neural remodeling during CNS development. Prolonged microglia activation and neuroinflammation are considered key contributors to neurological disorders. In this regard, it is becoming increasingly important to consider the potential influences underlying the crosstalk between the intestinal microbiota ecosystem and host when determining biomarkers of disease and treatment efficacy. The commensal microbiota is critical for immune development and continuous function through the recognition of bacteria-produced and regulated metabolites. In cases of microbial dysbiosis and microglial dysfunction, chronic neuroinflammation may persist, leading to the propagation of neurological disorders. To address potential mechanisms, this review focuses on the microbiota-gut-brain axis as it relates to communication pathways that have been linked to aberrant CNS immune activity and pathology. We also address anti-inflammatory and neuroprotective mediators which may counteract these detrimental activities. Finally, we explore the potential benefits of current and novel microbiome-targeted approaches to treat neuroinflammation and consequential neurological disease.