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Publisher: Smart Science and Technology LLC   (Total: 21 journals)   [Sort by number of followers]

Showing 1 - 21 of 21 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 8)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 6)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 2)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 14)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 2)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 1)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access  
Stem Cell and Translational Investigation     Open Access   (Followers: 2)
Stem Cell Epigenetics     Open Access   (Followers: 3)
Telomere and Telomerase     Open Access  
Therapeutic Targets for Neurological Diseases     Open Access  
Uterus & Ovary     Open Access  
Journal Cover Receptors & Clinical Investigation
  [1 followers]  Follow
    
  This is an Open Access Journal Open Access journal
   ISSN (Print) 2330-0566
   Published by Smart Science and Technology LLC Homepage  [21 journals]
  • CD28 family of receptors inter-connect in the regulation of T-cells

    • Authors: Janna Krueger, Felix Jules, Sadiye Reider, Christopher Rudd
      Abstract: T-cell activation is mediated by a combination of signals from the antigen receptor (TCR) and co-receptors such as CD28, cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed cell death antigen 1 (PD-1), CD28H and others.  Each is a member of the CD28 receptor gene family. CD28 sends positive signals that promote T-cell responses, while CTLA-4 and PD-1 limit responses. It is the balance between these positive and negative signals that determines the amplitude and level of T-cell responses.  The regulatory role of other family members is also becoming the focus of increasing interest.  The function of certain CD28 family members such as CTLA-4 and PD-1 is dependent the expression of CD28.  Together, these findings have important implications in generation of immune responses and the application of anti-receptor blocking reagents in immunotherapy. 
      PubDate: 2017-09-25
      DOI: 10.14800/rci.1581
      Issue No: Vol. 4, No. 3 (2017)
       
  • The role of leptin in the central nervous system remyelination

    • Authors: Ken Matoba, Rieko Muramatsu, Toshihide Yamashita
      Abstract: Leptin is identified as a mouse obesity gene, which is also preserved in humans. Leptin receptor is highly expressed in the hypothalamus relative to other tissues; therefore, the function of leptin is mainly attributed to hypothalamic control of food intake and body weight. Although the expression of leptin receptors is not limited to the hypothalamus but is also present in other regions of the central nervous system (CNS), such as the spinal cord, the functions of leptin and leptin receptor in the CNS have not been fully clarified. In this research highlight, we focus on the novel function of leptin in CNS remyelination in pathologic conditions, such as the demyelination mouse model. Because remyelination is a crucial process for repair of neuronal networks after injury and wound healing, knowledge of the underlying molecular mechanism of remyelination is useful to establish a therapeutic strategy against demyelinating diseases. We only revealed the role of leptin in remyelination at a histological level; however, a behavioral analysis and evidence of the beneficial effect of leptin for humans may add to knowledge of the effect of leptin on remyelination function.
      PubDate: 2017-08-14
      DOI: 10.14800/rci.1583
      Issue No: Vol. 4, No. 3 (2017)
       
  • Targeting sympathetic glia for treating cardiovascular diseases

    • Authors: Alison Xiaoqiao Xie, Angelo Chaia, Ken D. McCarthy
      Abstract: Gq G protein–coupled receptor (Gq-GPCR) signaling in Glial fibrillary acidic protein-expressing (GFAP+) glia is essential for neuron-glia interaction in the Central Nervous System (CNS). However, the exploration of the roles of Gq-GPCR signaling in peripheral GFAP+ glia has just begun. Our recent study showed that GFAP+ glia in the sympathetic ganglia, namely satellite glial cells (SGCs), positively modulate sympathetic-regulated cardiac functions following their Gq-GPCR activation. In this research highlight, we discuss the significance of satellite glial modulation of sympathetic nerve activity (SNA) in both physiology and in diseases. We also present a new experimental strategy for manipulating satellite glial signaling in the sympathetic ganglia using adeno-associated virus (AAV). The success of targeted viral transduction in ganglionic SGCs suggest a strong therapeutic potential of targeting sympathetic glia for the treatment of cardiovascular diseases (CVDs).
      PubDate: 2017-08-07
      DOI: 10.14800/rci.1572
      Issue No: Vol. 4, No. 3 (2017)
       
  • Computational analysis in Influenza virus

    • Authors: Rahul Dilip Chavan, Sanket Bapat, Vrushali Patil, Abhay Chowdhary, Avinash Kale
      Abstract: Influenza viruses are major human pathogens accountable for respiratory diseases affecting millions of people worldwide and characterized by high morbidity and significant mortality. Influenza infections can be controlled by vaccination and antiviral drugs. However, vaccines need yearly updating and give limited protection.  In addition, at presently available drugs suffer from the rapid and extensive emergence of drug resistance. All this highlights the urgent need for developing new antiviral strategies with novel mechanisms of action and with reduced drug resistance potential. Recent advances in the understanding of Influenza virus replication have discovered a number of cellular drug targets that counteract viral drug resistance.  With expanded bioinformatics’ knowledge on computational modeling and molecular dynamic stimulations, novel small molecule inhibitors of herbal/ayurvedic origin are being explored due to their non-toxicity and affordability. Using in-silico techniques the structural details and information of influenza protein have been studied to identify the potential drugs for inhibition. Further, we have discussed the various computational studies carried out on major protein/targets of Influenza which could provide new clues for a newer class of antiviral (ayurvedic) drugs. Therapy for influenza will go through significant changes in the decades to come, evolving with our knowledge of pathogenesis as new approaches become viable and are validated clinically.
      PubDate: 2017-07-31
      DOI: 10.14800/rci.1574
      Issue No: Vol. 4, No. 3 (2017)
       
  • HIF-1α promotes NSCs migration by modulating Slit2-Robo1 signaling
           after cerebral ischemia

    • Authors: Hua Ye, Min-rui Chen, Wan-fu Wu
      Abstract: Our previous studies have shown that transplantation of Hypoxia-inducible factor-1α (HIF-1α) gene modified neural stem cells (NSCs) reduced brain injury by improving the survival of NSCs and protecting the vascular system. HIF-1α plays pivotal roles during hypoxia, and its downstream pathways might be the primary mechanisms for the growth of NSCs. However, there are very few studies reported whether HIF-1α regulates NSCs migration. In this study, to test the hypothesis that HIF-1α modulates migration of NSCs after cerebral ischemia, we compared the injection of HIF-1α gene recombinant adenovirus, and control adenovirus in ischemia penumbra at 24 h after transient middle cerebral artery occlusion (tMCAO). BrdU labeled NSCs were transplanted in the lateral ventricle at the same time in both groups. The modified neurological severity score (NSS) was used to evaluate neurological deficits. Immunohistochemistry for HIF-1α, BrdU, Slit2 and Robo1 were performed. Comparing with vehicle group HIF-1α group showed better behavioral recovery on day 21 and 28. Expression of HIF-1α in HIF-1α group is higher than that in vehicle group. In HIF-1α group, more BrdU-positive cells were found than that in vehicle group. There are increased Slit2 in HIF-1α group. However, robo1, a receptor of Slits is decreased than that in vehicle group. Thus, we concluded that in cerebral ischemia rat model HIF-1α increased NSCs migration by inhibiting Slit2-Robo1 pathway, and improved the neurological behavior. In conclusion, our results indicate that HIF-1α may be a potential therapeutic target for ischemic stroke through promoting neuroregeneration.
      PubDate: 2017-06-26
      DOI: 10.14800/rci.1549
      Issue No: Vol. 4, No. 2 (2017)
       
  • Urokinase-type Plasminogen Activator (uPA) and its Receptor (uPAR) Promote
           Neurorepair in the Ischemic Brain

    • Authors: Paola Merino, Ariel Diaz, Manuel Yepes
      Abstract: Despite the fact that ischemic stroke has been considered a leading cause of mortality in the world,  recent advances in our understanding of the pathophysiological mechanisms underlying the ischemic injury and the treatment of acute ischemic stroke patients have led to a sharp decrease in the number of stroke deaths.  However, this decrease in stroke mortality has also led to an increase in the number of patients that survive the acute ischemic injury with different degrees of disability.  Unfortunately, to this date we do not have an effective therapeutic strategy to promote neurological recovery in these growing population of stroke survivors. Cerebral ischemia not only causes the destruction of a large number of axons and synapses but also activates endogenous mechanisms that promote the recovery of those neurons that survive its harmful effects.  Here we review experimental evidence indicating that one of these mechanisms of repair is the binding of the serine proteinase urokinase-type plasminogen activator (uPA) to its receptor (uPAR) in the growth cones of injured axons.  Indeed, the binding of uPA to uPAR in the periphery of growth cones of injured axons induces the recruitment of β1-integrin to the plasma membrane, β1-integrin-mediated activation of the small Rho GTPase Rac1, and Rac1-induced axonal regeneration.  Furthermore, we found that this process is modulated by the low density lipoprotein receptor-related protein (LRP1).  The data reviewed here indicate that the uPA-uPAR-LRP1 system is a potential target for the development of therapeutic strategies to promote neurological recovery in acute ischemic stroke patients.
      PubDate: 2017-06-06
      DOI: 10.14800/rci.1552
      Issue No: Vol. 4, No. 2 (2017)
       
  • An Entry-Competent Intermediate State of the HIV-1 Envelope Glycoproteins

    • Authors: Alon Herschhorn, Joseph Sodroski
      Abstract: The human immunodeficiency virus type 1 (HIV-1) envelope glycoproteins (Env) mediate viral entry and are the sole target of neutralizing antibodies. Recent studies show that the metastable HIV-1 Env trimer can transit among three conformational states: State 1, State 3, and State 2, corresponding to the “closed”, “open” and intermediate conformations, respectively. During virus entry, binding to the receptor, CD4, drives Env from state 1 to state 3.  In the unliganded Env, transitions from the closed (State 1) conformation are restrained by intramolecular interactions among different Env residues, which regulate HIV-1 Env conformation. Releasing the specific restraints on State 1 Env leads to increased occupancy of State 2, which is a functional conformation on the entry pathway and an obligate intermediate between State 1 and State 3. Frequent sampling of intermediate State 2 allows HIV-1 to infect cells expressing low levels of CD4, and leads to resistance to several broadly neutralizing antibodies and small-molecule inhibitors. Recent findings provide new mechanistic insights into the function and inhibition of HIV-1 Env and will contribute to ongoing therapeutic and prevention efforts to combat HIV-1.
      PubDate: 2017-05-24
      DOI: 10.14800/rci.1544
      Issue No: Vol. 4, No. 1 (2017)
       
  • G Protein-Coupled Receptors Mediate Neural Regulation of Innate Immune
           Responses in Caenorhabditis elegans

    • Authors: Yiyong Liu, Jingru Sun
      Abstract: G protein-coupled receptors (GPCRs) are a large family of transmembrane proteins that perceive many extracellular signals and transduce them into cellular physiological responses.  GPCRs regulate immunity in both vertebrates and invertebrates.  However, the mechanisms responsible for such regulation are not fully understood.  Recent research using the genetically tractable model organism Caenorhabditis elegans has led to the identification of specific GPCRs, neurotransmitters, neurons and non-neural cells in the regulation of innate immunity.  Several neural circuits have been demonstrated to function in GPCR-dependent immuno-regulatory pathways.  Besides being essential in neural-immune interactions, GPCRs also regulate innate immune response in non-neural tissues cell-autonomously through mechanisms independent of neural circuits.  Here we review GPCR-mediated neural control of innate immunity in C. elegans and briefly discuss GPCR-dependent immune regulation via non-neural mechanisms.
      PubDate: 2017-05-24
      DOI: 10.14800/rci.1543
      Issue No: Vol. 4, No. 1 (2017)
       
  • Bacterial superantigen toxins induce a lethal cytokine storm by enhancing
           

    • Authors: Raymond Kaempfer, Andrey Popugailo, Revital Levy, Gila Arad, Dalia Hillman, Ziv Rotfogel
      Abstract: Formation of the costimulatory axis between the B7-2 and CD28 coreceptors is critical for T-cell activation. Superantigens, Gram-positive bacterial virulence factors, cause toxic shock and sepsis by hyperinducing inflammatory cytokines. We report a novel role for costimulatory receptors CD28 and B7-2 as obligatory receptors for superantigens, rendering them therapeutic targets. We show that by engaging not only CD28 but also its coligand B7-2 directly, superantigens potently enhance the interaction between B7-2 and CD28, inducing thereby T-cell hyperactivation. Using a conserved twelve amino-acid domain, superantigens engage both B7-2 and CD28 at their homodimer interfaces, sites far removed from where these receptors interact, implying that inflammatory signaling can be controlled through the receptor homodimer interfaces. Short B7-2 and CD28 dimer interface mimetic peptides bind diverse superantigens, prevent superantigen binding to cell-surface B7-2 or CD28, attenuate inflammatory cytokine overexpression, and protect mice from lethal superantigen challenge. Thus, superantigens induce a cytokine storm by mediating not only the interaction between MHC-II molecule and T-cell receptor but critically, by promoting B7-2/CD28 coreceptor engagement, forcing the principal costimulatory axis to signal excessively. Our findings highlight the B7/CD28 interaction as a bottleneck in signaling for expression of inflammatory cytokines. B7-2 and CD28 homodimer interface mimetic peptides prevent superantigen lethality by blocking the superantigen-host costimulatory receptor interaction. 
      PubDate: 2017-01-30
      DOI: 10.14800/rci.1500
      Issue No: Vol. 4, No. 1 (2017)
       
  • Manuscript Preparation and Proofreading Guidelines

    • Authors: Editorial Office
      Abstract: More information can be found at Author Guidelines.
      DOI: 10.14800/rci.1155
      Issue No: Vol. 3, No. 1
       
 
 
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