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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: 11)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 8)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 3)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 16)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 3)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 2)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access   (Followers: 1)
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   (Followers: 1)
Uterus & Ovary     Open Access  
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Itch & Pain
Number of Followers: 2  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2377-9756
Published by Smart Science and Technology LLC Homepage  [21 journals]
  • Toll-like receptor 2 signaling induces interferon regulatory factor 8
           expression in spinal cord microglia after peripheral nerve injury

    • Authors: Hyoungsub Lim, Minsu Gwon, Sung Joong Lee
      Abstract: Although it is well known that spinal cord microglia activation plays a causal role in the development of neuropathic pain after peripheral nerve injury (PNI), the mechanisms of this activation have not been completely elucidated. We have previously shown that toll-like receptor 2 (TLR2) is involved in PNI-induced spinal cord microglia activation. A more recent study showed that PNI induces interferon regulatory factor 8 (IRF8), which is a key transcription factor responsible for microglia activation. In this study, we investigated the putative role of TLR2 in IRF8 expression in spinal cord microglia after PNI. In TLR2 knockout mice, nerve injury-induced spinal cord IRF8 expression was severely compromised. In addition, an intrathecal injection of lipoteichoic acid (LTA), a TLR2 agonist, induced IRF8 mRNA expression in the spinal cord. Lastly, TLR2 stimulation by LTA induced IRF8 mRNA expression in primary spinal cord glial cells. TLR2-induced IRF8 expression was dependent on p38 MAPK and NF-κB activation. Taken together, these data show that TLR2 activation induces IRF8 expression in spinal cord microglia after PNI.
      PubDate: 2017-01-02
      DOI: 10.14800/ip.1457
      Issue No: Vol. 3 (2017)
  • Successful treatment of persistent visual aura with lamotrigine

    • Authors: Hannah L. Kirsch, Kasra Maasumi
      PubDate: 2016-11-28
      DOI: 10.14800/ip.1458
      Issue No: Vol. 3 (2016)
  • Neuromediators for cholestatic pruritus

    • Authors: Hongzhen Hu
      Abstract: Cholestatic pruritus is one of the most common complaints in patients with liver diseases and intra- or post- hepatic cholestasis. The mechanisms of cholestatic pruritus remain poorly understood although multiple factors are considered to participate in the pathogenesis of cholestatic pruritus. Recent exciting studies have discovered several G-protein coupled receptors (GPCRs) and endogenous chemical ligands that play critical roles in mediating cholestatic pruritus in animal models and patients. These new findings have provided novel insights into the molecular and cellular mechanisms of cholestatic pruritus and improved our understanding of the etiology and treatment for the condition.
      PubDate: 2016-11-14
      DOI: 10.14800/ip.1451
      Issue No: Vol. 3 (2016)

    • Authors: Xian-Min Yu, Xing-Hong Jiang
      Abstract: Neurons in the trigeminal subnucleus caudalis (Vc) and spinal cord dorsal horn (SDH) play important roles in modulating and relaying pain signals to the higher centers of the central nervous system (CNS). Morphologically, many aspects including a laminated structure, cytoarchitecture and cellular elements in these two central regions are very similar [1,2,3,4]. Most nociceptive afferents with a small-diameter terminate in the superficial laminae of Vc and SDH. Functionally, sensory neurons in Vc and SDH respectively receive nociceptive inputs from the orofacial and other somatic regions, and convey the inputs to higher brain centers [1,2,3,4,5]. According to the mechanoreceptive properties, sensory neurons in both the Vc and SDH are classified into three types. They are low-threshold mechanoreceptive (LTM), wide-dynamic range (WDR) and nociceptive-specific neurons (NS) [1,2,3,4,5]. Because of these similarities Vc has been considered as analogous to SDH [4,6]. However, some differences between Vc and SDH have also been reported. For example, the distribution pattern of substance P (SP) and calcitonin gene related peptide (CGRP) in Vc of adult animals is different from that in SDH. In SDH there is no dual representation of peripheral regions, which can be found in rostral and caudal Vc. A transitional zone found between Vc and trigeminal subnucleus interpolaris plays a special role in sensorimotor function. However, no such region is found in the spinal system [5,7,8]. CNS neurons are regionalized. They are organized as groups through their circuitry. Although it is known that differences in functions among these groups in the adult CNS are predetermined during the development of the neuroepithelium [9,10,11,12,13], understanding how the regional specificity is developed in the CNS is still a big challenge in neuroscience research. It has recently been found that ninhydrin-reacting small molecules released locally are involved in the region-specific regulation of neuronal development in cultured Vc and SDH neurons [14,15]. In this review we focused on present knowledge about the region-specific regulation of neuronal development in these two CNS regions associated with the transmission of nociceptive signals.
      PubDate: 2016-06-13
      DOI: 10.14800/ip.1341
      Issue No: Vol. 3 (2016)
  • Research Highlights: Pain Control in Orthodontics Using Vibration

    • Authors: Wendy D. Lobre, William J. Dunn
      Abstract: Pain is a common patient complaint during the orthodontic movement of teeth, especially immediately following archwire placement.  Vibration has been used to accelerate the orthodontic movement of teeth and some observations by clinicians have indicated that vibration appeared to reduce the pain of orthodontic treatment.  The purpose of this parallel group, randomized clinical trial was to investigate the relationship between a micro pulse vibration device and pain perception during orthodontic treatment.  Fifty-eight patients meeting eligibility criteria were assigned using block allocation to one of two groups:  an experimental group using the vibration device or the control group (n = 29 for each group).  Patients used the device twenty minutes daily.  Patients rated pain intensity on a visual analog scale at appropriate intervals during the weeks after the separator or archwire appointment. Data were analyzed using repeated measures analysis of variance at α = .05.  Over the four month test period significant differences between the micro pulse vibration device group and the control group for overall pain (P =.002) and biting pain (P=.003) were identified.  The authors observed that perceived pain was highest at the beginning of the month, following archwire adjustment.  The micro pulse vibration device significantly lowered the pain scores for overall pain and biting pain over the four month study period. 
      PubDate: 2016-02-01
      DOI: 10.14800/ip.1165
      Issue No: Vol. 3 (2016)
  • Prostaglandin D2 improves IL-31-induced alloknesis: itch-stimulation
           becomes pain-stimulation in mouse skin

    • Authors: Iwao Arai, Minoru Tsuji, Kazuya Miyagawa, Hiroshi Takeda, Nobutake Akiyama, Saburo Saito
      Abstract: We examined the effect of prostaglandin D2 (PGD2) on IL-31-induced alloknesis in mice. We investigated itch-associated scratching behavior (long-lasting scratching: LLS) as an indicator of itching. Topically applied PGD2 and dexamethasone each significantly suppressed IL-31 (acute or repeated administration)-induced LLS.  However, neither PGD2 nor dexamethasone suppressed the IL-31 (repeated administration)-induced increase in IL-31 receptor A mRNA expression in dorsal root ganglia. Next, we investigated the scratching behavior induced by pruritogens (histamine, serotonin and compound 48/80) or algogens (acetylcholine, bradykinin and capsaicin) in IL-31-induced itchy-skin mice. In naïve mice, these irritants caused many counts of short-lasting scratching (SLS) and a few counts of LLS for 60 min. In contrast, IL-31-induced itchy-skin mice showed significant increases in LLS counts compared with naïve mice. Topical application of PGD2 significantly suppressed LLS counts induced by these pruritogens or algogens in IL-31-induced itchy-skin mice. The anti-pruritic efficacy of PGD2 may be related to its ability to reverse the hyperkinesis of primary afferents; thus, PGD2 improves IL-31-induced alloknesis. In a hot-plate test, topical application of PGs (PGD2, PGE2 and PGI2) caused a decrease in the nociceptive threshold in naïve mice, indicating that PGs enhance pain. These results suggest that PGs (especially PGD2) can change itch-stimulation into pain-stimulation in itchy-skin mice caused by pretreatment with IL-31. Therefore, it is possible that IL-31 and PGs may play a role in the regulation of a primary sensory nerves for the sensation of itch and pain.
      PubDate: 2016-01-12
      DOI: 10.14800/ip.1138
      Issue No: Vol. 3 (2016)

    • Authors: Arzu Yagiz On
      Abstract: The question whether Fibromyalgia syndrome (FMS) is a distinct clinical entity in the context of chronic widespread pain (CWP) have remained challenging after decades of research and several diagnostic criteria that have attempted to clarify FMS. A recent study has raised more challenges on the issue, proposing that diagnosis of FMS in patients representing with CWP is not informative or helpful for clinical practice and such a differentiation will provide little or no significance regarding the choice of effective and safe therapies. This proposal will be further discussed here by reviewing the recent advances in the field of pain medicine. These advances have collectively provided compelling evidence that all individuals with chronic pain, even those classically categorized as originating from peripheral/nociceptive origins have common central contributions to their pain and associated comorbidities. The recent understanding of the pain mechanisms has also provided important implications on classification and management of pain. Centrally acting agents have been recommended as first-line treatment options for FMS and potential use of these agents has been expanded to other chronic pain disorders. After having reviewed the recent advances in the pain field, distinction between CWP and FMS still seems not to be useful in clinical practice, as effective treatment in an individual patient might be much guided by dominant underlying mechanisms rather than specific diagnosis the patient is suffering. The conditions representing with CWP in the absence of definitive objective confirmation may then be classified under one heading such as “CWP”, “chronic pain syndrome” or “central pain”, when considering their similar pattern of clinical presentation, commonality of central sensitization to their pathophysiology and their similar response to centrally acting analgesics.  Future research should be directed toward classification of CWP based on the validated measurements of different aspects of pain.  Such a classification may help clinicians identify the patients who will preferentially respond to peripheral or centrally acting analgesics and may therefore assist in advancing a more individualized and pain mechanism focused treatment in the clinical setting. 
      PubDate: 2016-01-04
      DOI: 10.14800/ip.1079
      Issue No: Vol. 3 (2016)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762
Fax: +00 44 (0)131 4513327
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