Pain Management of Herpes Zoster

Herpes zoster (HZ) is a disease triggered by the reactivation of latent varicella zoster virus (VZV) in spinal or cranial sensory ganglia, and is characterized by a painful vesicular eruption in the affected dermatome. Postherpetic neuralgia (PHN) is a chronic, neuropathic pain that can persist long beyond resolution of visible cutaneous manifestations which is often resistant to current analgesic treatments. The lifetime prevalence of herpes zoster is approximately 20–30% and about 9–34% of these patients develop PHN depending on its definition. Clinical experience has shown that PHN often develops in cases of inadequate initial pain management resulting in increased pain intensity. This review provides an overview of the treatment options for HZ and PHN, focusing on the therapeutic modalities of pain management. The primary objectives of management of HZ are to inhibit viral replication, relieve pain, and prevent associated complications, such as PHN. General treatments for acute HZ are combination of antiviral therapy with a short course of corticosteroids at the onset of the disease in conjunction with an effective control of acute pain, including nonsteroidal anti-inflammatory drugs, acetaminophen, opioids, and anticonvulsants such as gabapentin or pregabalin. Treatment of PHN is often resistant to the current pharmacologic methods. Therefore, a multimodal analgesic treatment regimen including topical lidocaine and capsaicin, systemic therapies, and the interventional treatments is necessary to alleviate pain and its effect on quality of life. As the incidence of HZ increases with age, the number of patients with HZ and PHN may increase in the future considering the gradual aging of the general population. Appropriate management of HZ can reduce the duration and intensity of pain from HZ, and prevent the development of PHN. In addition, prophylactic zoster vaccination can prevent or reduce the incidence of HZ and PHN. Further efforts are needed to minimize pain of the patients suffering from HZ and PHN as it affects the quality of life in the aspect of both physical and psychological impairments

Comparison of air pollution and the prevalence of allergy-related diseases in Incheon and Jeju City

PurposeA high level of air pollutants can increase the number of patients with allergy-related diseases such as asthma and allergic rhinitis (AR). To analyze the association between air pollution and allergic disease, we investigated 2 areas in Korea: Incheon, an industrial area, and Jeju, a non-industrialized area.MethodsSecond grade students at elementary schools (11 schools in Incheon and 45 schools in Jeju) were examined in a cross-sectional study. A questionnaire was used and a skin prick test was performed. The levels of NO2, CO2, O3, particulate matter (PM) PM10/2.5, formaldehyde, tVOCs, and dust mites in the classrooms and grounds were determined.ResultsThe levels of outdoor CO, PM10, and PM2.5 were significantly higher in Incheon (P<0.01). The levels of indoor CO, CO2, PM10, PM2.5 were significantly higher in Incheon (P<0.01). The prevalence rates of AR symptoms at any time, AR symptoms during the last 12 months, diagnosis of rhinitis at any time, and AR treatment during the last 12 months were significantly higher in Incheon (P<0.01). The prevalence rate of wheezing or whistling at any time, and wheezing during the last 12 months were significantly higher in Incheon (P<0.01).ConclusionWe found that the children living in Incheon, which was more polluted than Jeju, had a higher rate of AR and asthma symptoms compared to children in Jeju. To determine the effect of air pollution on the development of the AR and asthma, further studies are needed

The Expression of Matrix Metalloprotease 20 is Stimulated by Wild Type but not by 4 bp- or 2 bp- Deletion Mutant DLX3

Mutations in DLX3 are associated with both autosomal dominant hypoplastic hypomaturation amelogenesis imperfecta (ADHHAI) and tricho-dento-osseous (TDO) syndrome. ADHHAI is caused by a c.561_562delCT (2bpdel DLX3) mutation whereas TDO syndrome is associated with a c.571_574delGGGG (4bp-del DLX3) mutation. However, although the causal relationships between DLX3 and an enamel phenotype have been established, the pathophysiological role of DLX3 mutations in enamel development has not yet been clarified. In our current study, we prepared expression vectors for wild type and deletion mutant DLX3 products (4bp-del DLX3, 2bp-del DLX3) and examined the effects of their overexpression on the expression of the enamel matrix proteins and proteases. Wild type DLX3 enhanced the expression of matrix metalloprotease 20 (MMP20) mRNA and protein in murine ameloblast-like cells. However, neither a 4bp-del nor 2bpdel DLX3 increased MMP20 expression. Wild type DLX3, but not the above DLX3 mutants, also increased the activity of reporters containing 1.5 kb or 0.5 kb of the MMP20 promoter. An examination of protein stability showed that the half-life of wild type DLX3 protein was less than 12 h whilst that of both deletion mutants was longer than 24 h. Endogenous Dlx3 was also found to be continuously expressed during ameloblast differentiation. Since inactivating mutations in the gene encoding MMP20 are associated with amelogenesis imperfecta, the inability of 4bp-del or 2bp-del DLX3 to induce MMP20 expression suggests a possible involvement of such mutations in the enamel phenotype associated with TDO syndrome or ADHHAI

Growth differentiation factor 11 locally controls anterior-posterior patterning of the axial skeleton.

Growth and differentiation factor 11 (GDF11) is a transforming growth factor β family member that has been identified as the central player of anterior-posterior (A-P) axial skeletal patterning. Mice homozygous for Gdf11 deletion exhibit severe anterior homeotic transformations of the vertebrae and craniofacial defects. During early embryogenesis, Gdf11 is expressed predominantly in the primitive streak and tail bud regions, where new mesodermal cells arise. On the basis of this expression pattern of Gdf11 and the phenotype of Gdf11 mutant mice, it has been suggested that GDF11 acts to specify positional identity along the A-P axis either by local changes in levels of signaling as development proceeds or by acting as a morphogen. To further investigate the mechanism of action of GDF11 in the vertebral specification, we used a Cdx2-Cre transgene to generate mosaic mice in which Gdf11 expression is removed in posterior regions including the tail bud, but not in anterior regions. The skeletal analysis revealed that these mosaic mice display patterning defects limited to posterior regions where Gdf11 expression is deficient, whereas displaying normal skeletal phenotype in anterior regions where Gdf11 is normally expressed. Specifically, the mosaic mice exhibited seven true ribs, a pattern observed in wild-type (wt) mice (vs. 10 true ribs in Gdf11-/- mice), in the anterior axis and nine lumbar vertebrae, a pattern observed in Gdf11 null mice (vs. six lumbar vertebrae in wt mice), in the posterior axis. Our findings suggest that GDF11, rather than globally acting as a morphogen secreted from the tail bud, locally regulates axial vertebral patterning

Influence of the surface roughness on inner-outer interactions in a turbulent Couette-Poiseuille flow

When rod surface roughness is introduced in a turbulent Couette-Poiseuille flow (CP-flow), it is known that the Reynolds stresses near the centerline decrease due to weakened very-large-scale motions (VLSMs) and roll-cell motions [Lee, Y. M. et al., &quot;Direct numerical simulation of a turbulent Couette-Poiseuille flow with a rod-roughened wall,&quot; Phys. Fluids 30, 105101 (2018)]. In the present study, we examine the origin of the weakened turbulent structures near the centerline in a CP-flow with roughness (CPR-flow) using a dataset from direct numerical simulation. The top-down and bottom-up interactions to organize a CP-flow are very similar to those found in earlier studies in turbulent channel/pipe and boundary layer flows. The circulation of roll-cells in the outer region induces the spanwise congregation of negative streamwise velocity fluctuating structures (u) near the wall, leading to a large-scale ejection into the outer region. This large-scale ejection contributes to the formation of a negative VLSM when two adjacent negative large-scale motions merge, and the VLSM induces the circulation of roll-cell motion due to the pure kinematics. A similar process for the inner-outer interactions is found for a CPR-flow. However, because the impact of the surface roughness suppresses the collective motion of negative u-structures near the surface roughness, strong congregation by roll-cells is observed to occur far from the wall, indicating that relatively few negative u-structures with low strength contribute to the formation of a large-scale ejection for the CPR-flow. The weakened large-scale ejection decreases the strength of the VLSM, resulting in weakened roll-cell motion

Analysis of the Relationship between Cerebellar Volume and Psychological Parameters in 20s Male Adults

AbstractThis study measured the cerebellar volume of normal male adults in 20s with magnetic resonance imaging (MRI) and analysed the relationship between cerebellar volume and various psychological parameters. The cerebellar volume of 58 males (mean age, 24.0-2.8 years) was measured using MRI. The Symptom Checklist-90-R (SCL-90-R) and the Component of Type A Behavior tests were performed. Using linear regression analysis, the relationship between cerebellar volume and psychological parameters was analysed. As phobic anxiety and ambition increased, cerebellar volume of normal male subjects in 20s decreased. This study showed that for even normal male adults, there exists a possible relationship between various psychological parameters and cerebellar volume

Angiographic and Clinical Result of Endovascular Treatment in Paraclinoid Aneurysms

PurposeThe purpose of this study was to analyze the results of an immediate and mid-term angiographic and clinical follow-up of endovascular treatment for paraclinoid aneurysms.Materials and MethodsFrom January 2002 to December 2012, a total of 113 consecutive patients (mean age: 56.2 years) with 116 paraclinoid saccular aneurysms (ruptured or unruptured) were treated with endovascular coiling procedures. Clinical and angiographic outcomes were retrospectively evaluated.ResultsNinety-three patients (82.3%) were female. The mean size of the aneurysm was 5.5 mm, and 101 aneurysms (87.1%) had a wide neck. Immediate catheter angiography showed complete occlusion in 40 aneurysms (34.5%), remnant sac in 51 (43.9%), and remnant neck in 25 (21.6%). Follow-up angiographic studies were performed on 80 aneurysms (69%) at a mean period of 20.4 months. Compared with immediate angiographic results, follow-up angiograms showed no change in 38 aneurysms, improvement in 37 (Fig. 2), and recanalization in 5. There were 6 procedure-related complications (5.2%), with permanent morbidity in one patient.ConclusionOut study suggests that properly selected patients with paraclinoid aneurysms can be successfully treated by endovascular means

High Extracellular Calcium Increased Expression of Ank, PC-1 andOsteopontin in Mouse Calvarial Cells

In the process of bone remodeling, mineral phase of bone is dissolved by osteoclasts, resulting in elevation of calcium concentration in micro-environment. This study was performed to explore the effect of high extracellular calcium (Ca 2+ e) on mineralized nodule formation and on the expression of progressive ankylosis (Ank), plasma cell membrane glycoprotein-1 (PC-1) and osteopontin by primary cultured mouse calvarial cells. Osteoblastic differentiation and mineralized nodule formation was induced by culture of mouse calvarial cells in osteoblast differentiation medium containing ascorbic acid and β-glycerophosphate. Although Ank, PC-1 and osteopontin are well known inhibitors of mineralization, expression of these genes were induced at the later stage of osteoblast differentiation during when expression of osteocalcin, a late marker gene of osteoblast differentiation, was induced and mineralization was actively progressing. High Ca 2+ e (10 mM) treatment highly enhanced mRNA expression of Ank, PC-1 and osteopontin in the late stage of osteoblast differentiation but not in the early stage. Inhibition of p44/42 MAPK activation but not that of protein kinase C suppressed high Ca 2+ e-induced expression of Ank, PC-1 and osteopontin. When high Ca 2+ e (5 mM or 10 mM) was present in culture medium during when mineral deposition was actively progressing, matrix calcifiation was significantly increased by high Ca 2+ e. This stimulatory effect was abolished by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an alkaline phosphatase inhibitor. In addition, probenecid (2mM), an inhibitor of Ank, suppressed matrix calcification in both control and high Ca 2+ e-treated group, suggesting the possible role of Ank in matrix calcification by osteoblasts. Taken together, these results showed that high Ca 2+ e stimulates expression of Ank, PC-1 and osteopontin as well as matrix calcification in late differentiation stage of osteoblasts and that p44/42 MAPK activation is involved in high Ca 2+ e- induced expression of Ank, PC-1 and osteopontin

Mesenchymal stem/stromal cells precondition lung monocytes/macrophages to produce tolerance against allo- and autoimmunity in the eye

Intravenously administered mesenchymal stem/stromal cells (MSCs) engraft only transiently in recipients, but confer long-term therapeutic benefits in patients with immune disorders. This suggests that MSCs induce immune tolerance by long-lasting effects on the recipient immune regulatory system. Here, we demonstrate that i.v. infusion of MSCs preconditioned lung monocytes/macrophages toward an immune regulatory phenotype in a TNF-α–stimulated gene/protein (TSG)-6–dependent manner. As a result, mice were protected against subsequent immune challenge in two models of allo- and autoimmune ocular inflammation: corneal allotransplantation and experimental autoimmune uveitis (EAU). The monocytes/macrophages primed by MSCs expressed high levels of MHC class II, B220, CD11b, and IL-10, and exhibited T-cell–suppressive activities independently of FoxP3(+) regulatory T cells. Adoptive transfer of MSC-induced B220(+)CD11b(+) monocytes/macrophages prevented corneal allograft rejection and EAU. Deletion of monocytes/macrophages abrogated the MSC-induced tolerance. However, MSCs with TSG-6 knockdown did not induce MHC II(+)B220(+)CD11b(+) cells, and failed to attenuate EAU. Therefore, the results demonstrate a mechanism of the MSC-mediated immune modulation through induction of innate immune tolerance that involves monocytes/macrophages