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Kalirin-7 contributes to type 2 diabetic neuropathic pain via the postsynaptic density-95/N-methyl-D-aspartate receptor 2B-dependent N-methyl-D-aspartate receptor 2B phosphorylation in the spinal cord in rats.

Diabetic neuropathic pain (DNP) is one of the common complications in type 2 Diabetes Mellitus (DM) patients. However, molecular mechanisms in underlying diabetic neuropathic pain are still poorly understood. Kalirin-7, a multifunctional Rho GDP/GTP exchange factor, located at the excitatory synapses, was reported to modulate the neuronal cytoskeleton. Therefore, in this study, we explored the effects of Kalirin-7 on type 2 diabetic neuropathic pain and the mechanisms in spinal cord in rats.

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The Prevalence of Restless Legs Syndrome in Patients with Migraine: A Systematic Review and Meta-Analysis.

Migraine is a severe and debilitating neurologic disorder and is claimed to be the sixth disabling illness in the world. This study aimed to determine the overall prevalence of restless legs syndrome (RLS) in patients with migraine through a systematic review and meta-analysis.

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A Case Report of Parry-Romberg Syndrome Misdiagnosed as Multiple Sclerosis.

Parry-Romberg syndrome (PRS) is a rare disease that causes hemiatrophy of the face. The pathophysiological mechanisms involved in its etiology are unknown, but several previous reports suggest the involvement of autoimmune factors. Herein we describe the case of a patient with PRS who was initially misdiagnosed as having multiple sclerosis (MS). The relevant literature is briefly reviewed, and some previous reports suggesting associations between PRS and autoimmunity are discussed. A 34-year-old man presented with recurrent paroxysmal weakness of the right hand, a 3-years history of unilateral tinnitus, and headache for 6 months. MS was initially diagnosed but the patient was subsequently diagnosed as having PRS on the basis of clinical manifestations and radiological findings. PRS may be associated with autoimmune pathogenesis, but the present case does not support that theory.

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2-O-Methylmagnolol, a Magnolol Derivative, Suppresses Hepatocellular Carcinoma Progression via Inhibiting Class I Histone Deacetylase Expression.

is widely used in Southeast Asian countries for the treatment of fever, headache, diarrhea, and stroke. Magnolol is a phenolic compound extracted from , with proven antibacterial, antioxidant, anti-inflammatory, and anticancer activities. In this study, we modified magnolol to synthesize a methoxylated derivative, 2-O-methylmagnolol (MM1), and investigated the use of MM1, and magnolol in the treatment of liver cancer. We found that both magnolol and MM1 exhibited inhibitory effects on the growth, migration, and invasion of hepatocellular carcinoma (HCC) cell lines and halted the cell cycle at the G1 phase. MM1 also demonstrated a substantially better tumor-suppressive effect than magnolol. Further analysis suggested that by inhibiting class I histone deacetylase expression in HCC cell lines, magnolol and MM1 induced p21 expression and p53 activation, thereby causing cell cycle arrest and inhibiting HCC cell growth, migration, and invasion. Subsequently, we verified the significant tumor-suppressive effects of magnolol and MM1 in an animal model. Collectively, these findings demonstrate the anti-HCC activities of magnolol and MM1 and their potential for clinical use.

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A Response to: Comparison of Psychological Difficulties in Patients with Migraine and Epilepsy Using PARADISE-24 Questionnaire [Letter].

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Telemedicine in the OECD: An umbrella review of clinical and cost-effectiveness, patient experience and implementation.

Patients and policy makers alike have high expectations for the use of digital technologies as tools to improve health care service quality at a sustainable cost. Many countries within the Organisation for Economic Co-operation and Development (OECD) are investing in telemedicine initiatives, and a large and growing body of peer-reviewed studies on the topic has developed, as a consequence. Nonetheless, telemedicine is still not used at scale within the OECD. Seeking to provide a snapshot of the evidence on the use of telemedicine in the OECD, this umbrella review of systematic reviews summarizes findings on four areas of policy relevance: clinical and cost-effectiveness, patient experience, and implementation.

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Transient Eosinophilic Granulomatosis with Polyangiitis-Like Vasculitis During Omalizumab Therapy: A Case Report.

A 67-year-old Caucasian female presented in August 2019 to our rheumatology service, with 3 days history of severe neck pain and right-sided headache with aches in both shoulders and arms and mild stiffness. Other symptoms included mild jaw claudication. She had recently returned from Majorca after an uneventful two-week trip. She had a background of severe allergic asthma and allergic rhinitis, well controlled with omalizumab which was started in 2016, based on persistently high IgE. Her sister suffers from a type of vasculitis and is currently on steroids. The patient is an ex-smoker and drinks two bottles of wine a week. She had high inflammatory markers with raised eosinophilic count and was admitted for further work up to rule out infection and to commence steroid after for a likely diagnosis of eosinophilic granulomatosis with polyangiitis. Shortly after admission to the acute assessment unit, she became confused and febrile. An extensive work up ruled out infection, and she was started on steroids and treated for acute hyponatremia. Omalizumab was stopped. She improved and was discharged on a tapering dose of steroids and was weaned off completely within 4 months. Her inflammatory markers returned to normal as well as her eosinophilic count, with complete resolution of her presenting symptoms.

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Danoprevir for the Treatment of Hepatitis C Virus Infection: Design, Development, and Place in Therapy.

On June 8, 2018, an NS3/4A protease inhibitor called danoprevir was approved in China to treat the infections of HCV genotype (GT) 1b – the most common HCV genotype worldwide. Based on phase 2 and 3 clinical trials, the 12-week regimen of ritonavir-boosted danoprevir (danoprevir/r) plus peginterferon alpha-2a and ribavirin offered 97.1% (200/206) of sustained virologic response at post-treatment week 12 (SVR12) in treatment-naïve non-cirrhotic patients infected with HCV genotype 1b. Adverse events such as anemia, fatigue, fever, and headache were associated with the inclusion of peginterferon alpha-2a and ribavirin in the danoprevir-based regimen. Moreover, drug resistance to danoprevir could be traced to amino acid substitutions (Q80K/R, R155K, D168A/E/H/N/T/V) near the drug-binding pocket of HCV NS3 protease. Despite its approval, the clinical use of danoprevir is currently limited to its combination with peginterferon alpha-2a and ribavirin, thereby driving its development towards interferon-free, ribavirin-free regimens with improved tolerability and adherence. In the foreseeable future, pan-genotypic direct-acting antivirals with better clinical efficacy and less adverse events will be available to treat HCV infections worldwide.

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The Actions and Mechanisms of P2X7R and p38 MAPK Activation in Mediating Bortezomib-Induced Neuropathic Pain.

The proteasome inhibitor bortezomib (BTZ) is a potent first-line anticancer drug for multiple myeloma; nonetheless, it induced peripheral neuropathy. It has been suggested that many cytokines may play a role in mediating neuropathic pain, but the underlying molecular mechanism is not fully understood. Recent studies have shown that neuropathic pain is closely related to the purinergic ligand-gated ion channel 7 receptor (P2X7R), one of the P2X receptors, which is richly expressed in glial cells. P2X7-p38 pathway is correlated with microglia- and satellite glial cell- (SGC-) mediated neuropathic pain. However, the association of P2X7R and p38MAPK in mediating BTZ-induced neuropathic pain remains unclear. In this study, the relationship between P2X7R activation and p38 phosphorylation in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) in the development and maintenance of BTZ-induced neuropathic pain was elucidated. The results showed that BTZ increased mechanical thresholds in rats, accompanied with upregulation of P2X7R expression and p38MAPK phosphorylation, indicating that P2X7R and p38MAPK are key molecules in the development and maintenance of BTZ-induced neuropathic pain. Inhibiting p38MAPK phosphorylation with SB203580 resulted in downregulation of P2X7R expression levels. Inhibition of P2X7R with Brilliant Blue G (BBG) reversed neuropathic pain might decrease through the expression of tumor necrosis factor- (TNF-), interleukin-1 (IL-1), and IL-6 via inhibiting p38MAPK phosphorylation. The P2X7R/p38MAPK signaling pathway in SGCs of DRG and microglia of SDH might be a potential pharmacological target behind this mechanism as an opportunity to relieve BTZ-induced neuropathic pain.

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Modifying MSC Phenotype to Facilitate Bone Healing: Biological Approaches.

Healing of fractures and bone defects normally follows an orderly series of events including formation of a hematoma and an initial stage of inflammation, development of soft callus, formation of hard callus, and finally the stage of bone remodeling. In cases of severe musculoskeletal injury due to trauma, infection, irradiation and other adverse stimuli, deficient healing may lead to delayed or non-union; this results in a residual bone defect with instability, pain and loss of function. Modern methods of mechanical stabilization and autologous bone grafting are often successful in achieving fracture union and healing of bone defects; however, in some cases, this treatment is unsuccessful because of inadequate biological factors. Specifically, the systemic and local microenvironment may not be conducive to bone healing because of a loss of the progenitor cell population for bone and vascular lineage cells. Autologous bone grafting can provide the necessary scaffold, progenitor and differentiated lineage cells, and biological cues for bone reconstruction, however, autologous bone graft may be limited in quantity or quality. These unfavorable circumstances are magnified in systemic conditions with chronic inflammation, including obesity, diabetes, chronic renal disease, aging and others. Recently, strategies have been devised to both mitigate the necessity for, and complications from, open procedures for harvesting of autologous bone by using minimally invasive aspiration techniques and concentration of iliac crest bone cells, followed by local injection into the defect site. More elaborate strategies (not yet approved by the U.S. Food and Drug Administration-FDA) include isolation and expansion of subpopulations of the harvested cells, preconditioning of these cells or inserting specific genes to modulate or facilitate bone healing. We review the literature pertinent to the subject of modifying autologous harvested cells including MSCs to facilitate bone healing. Although many of these techniques and technologies are still in the preclinical stage and not yet approved for use in humans by the FDA, novel approaches to accelerate bone healing by modifying cells has great potential to mitigate the physical, economic and social burden of non-healing fractures and bone defects.

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