Programmed cell death and natural killer cells in multiple sclerosis: new potential therapeutic targets?

Multiple sclerosis（MS）is a chronic,severe and complex disease of still uncertain etiopathogenesis,with lesions in the cerebral white matter and spinal cord.The disease is heterogeneous,but is characterized by neuroinflammatory and neurodegenerative processes,usually associated with altered activation of the immune system following presumable stimulation by still unknown autoantigens.

Consequences of hepatic damage after traumatic brain injury: current outlook and potential therapeutic targets

Traumatic brain injury（TBI）triggers liver inflammation：TBI is a serious pathology affecting around 10 million people annually,being a persistent public health and medical problem Forceful impact while playing sports,falls,physical assault,or traffic accidents are common causes of head injury.

The Olfactory Receptor Pseudo-pseudogene: A Potential Therapeutic Target in Human Diseases

Recently, Prieto-Godino et al.[1] found that the olfactory receptor 75a （Ir75a） gene is a functional pseudo-pseudogene in Drosophila sechellia. For a long time, Ir75a has been regarded as an acetic acid receptor that detects acetic acid and induces obvious olfactory responses in olfactory sensory neurons （OSNs）f2J. Nonetheless, Prieto-Godino et al. confirmed that Ir75a lost its sensitivity to acetic acid in D. sechellia. Thus, the D. sechelfia Ir75a gene is generally recognized as a pseudogene in OSNs.

Relevance and therapeutic potential of Cyp A targeting to block apoptosis inducing factor-mediated neuronal cell death

Programmed cell death （PCD） signaling pathways are import- ant contributors to acute neurological insults such as hypox- ic-ischemic brain damage, traumatic brain injury, stroke etc. The pathogenesis of all these diseases is closely linked with ab- erration of apoptotic cell death pathways. Mitochondria play a crucial role during PCD, acting as both sensors of death signals, and as initiators of biochemical path- ways, which cause cell death （Bras et al., 2005）. Cytochrome c was the firstly identified apoptogenic factor released from mitochondria into the cytosol, where it induces apoptosome formation through the activation of caspases. Other proteins, such as apoptosis inducing factor （AIF）, have been subsequently identified as mitochondrial released factors. AIF contributes to apoptotic nuclear DNA damage （Bras et al., 2005）. in a caspase-independent way

MicroRNA-216a: a potential therapeutic target for drug resistance and recurrent of liver cancer

The Editor welcomes submissions for possible publication in the Letters to the Editor section.Letters commenting on an article published in the Journal or other interesting pieces will be considered if they are received within 6 weeks of the time the article was published.Authors of the article being commented on will be given an opportunity to offer a timely response to the letter.Authors of letters will be notified that the letter has been received.Unpublished letters cannot be returned.

The Mitochondrion:A Potential Therapeutic Target for Alzheimer's Disease

Introduction The mitochondrion is a double-membrane organelle consisting of an outer membrane, intermembrane space, inner membrane, cristae, and matrix. It is the ‘‘energy plant’’ that provides most of the energy for cells. Mitochondria also participate in various processes such as calcium homeosta-