A novel assessment of abdominal pseudohernia after thoracolumbar vertebral compression fractures using surface electromyography and ultrasonography: A case report

Rationale:An abdominal pseudohernia is a protrusion of the abdominal wall that there is no actual muscular disruption. This report presents a case in which abdominal muscle activities were accurately and quantitatively measured using ultrasonography (US) and surface electromyography in a patient with abdominal pseudohernia.Patient concerns:A 62-year-old man presented with a marked protrusion on the left abdomen with increasing abdominal pressure.Diagnoses:First, the thickness of the abdominal muscle was measured with US while the patient constantly blew the positive expiratory pressure device. When the force was applied to the abdomen, the mean thickness of the muscle layer on the lesion site was found to be thinner. Second, the activities of the abdominal muscles were measured using surface electromyography by attaching electrodes to 8 channels at the same time. When the same pressure was applied on both sides of the abdomen, more recruitment occurred to compensate for muscle weakness at the lesion site. Through the previous 2 tests, the decrease in muscle activity in the lesion area could be quantitatively evaluated. Third, the denervation of the muscle was confirmed using US-guided needle electromyography.Interventions:The patient in this case was wearing an abdominal binder. In addition, he had been training his abdominal muscles through McGill exercise and breathing exercises such as with a positive expiratory pressure device.Outcomes:The patient was able to understand his symptoms. A follow-up test will be performed to see if there is any improvement.Lessons:By using these outstanding assessment methods, proper diagnosis and rehabilitation treatment strategies can be developed.     

Population Pharmacokinetic Modeling of the Enterohepatic Recirculation of Fimasartan in Rats,Dogs, and Humans

Enterohepatic recirculation (EHC) can greatly enhance plasma drug exposures and therapeutic effects. This study aimed to develop a population pharmacokinetic model that can simultaneously characterize the extent and time-course of EHC in three species using fimasartan, a novel angiotensin II receptor blocker, as a model drug. All fimasartan plasma concentration profiles in 32 rats (intravenous doses, 0.3–3 mg/kg; oral doses, 1–10 mg/kg), 34 dogs (intravenous doses, 0.3–1 mg/kg; oral doses, 1–10 mg/kg), and 42 healthy volunteers (single or multiple oral doses, 20–480 mg) were determined via liquid chromatography-tandem mass spectrometry (LC-MS/MS) and simultaneously modeled in S-ADAPT. The proposed model quantitatively characterized EHC in three species after oral and intravenous dosing. The median (range) fraction of drug undergoing recirculation was 76.3% (64.9–88.7%) in rats, 33.3% (24.0–45.9%) in dogs, and 65.6% (56.5–72.0%) in humans. In the presence compared with the absence of EHC, the area under the curve in plasma was predicted to be 4.22-fold (2.85–8.85) as high in rats, 1.50-fold (1.32–1.85) in dogs, and 2.91-fold (2.30–3.57) in humans. The modeled oral bioavailability in rats (median (range), 38.7% (20.0–59.8%)) and dogs (median, 7.13% to 15.4%, depending on the formulation) matched the non-compartmental estimates well. In humans, the predicted oral bioavailability was 25.1% (15.1–43.9%) under fasting and 18.2% (12.2–31.0%) under fed conditions. The allometrically scaled area under the curve predicted from rats was 420 ng ⋅ h/mL for 60 mg fimasartan compared with 424 ± 63 ng ⋅ h/mL observed in humans. The developed population pharmacokinetic model can be utilized to characterize the impact of EHC on plasma drug exposure in animals and humans.

Electronic supplementary material

The online version of this article (doi:10.1208/s12248-015-9764-2) contains supplementary material, which is available to authorized users.KEY WORDS: animal to human scaling, enterohepatic recirculation, fimasartan, population pharmacokinetics, S-ADAPT     

Civic Participation and Self-rated Health: A Cross-national Multi-level Analysis Using the World Value Survey

Objectives:

Civic participation, that which directly influences important decisions in our personal lives, is considered necessary for developing a society. We hypothesized that civic participation might be related to self-rated health status.

Methods:

We constructed a multi-level analysis using data from the World Value Survey (44 countries, n=50 859).

Results:

People who participated in voting and voluntary social activities tended to report better subjective health than those who did not vote or participate in social activities, after controlling for socio-demographic factors at the individual level. A negative association with unconventional political activity and subjective health was found, but this effect disappeared in a subset analysis of only the 18 Organization for Economic Cooperation and Development (OECD) countries. Moreover, social participation and unconventional political participation had a statistically significant contextual association with subjective health status, but this relationship was not consistent throughout the analysis. In the analysis of the 44 countries, social participation was of borderline significance, while in the subset analysis of the OECD countries unconventional political participation was a stronger determinant of subjective health. The democratic index was a significant factor in determining self-rated health in both analyses, while public health expenditure was a significant factor in only the subset analysis.

Conclusions:

Despite the uncertainty of its mechanism, civic participation might be a significant determinant of the health status of a country.     

Protective role of caffeic acid in an Aβ25-35-induced Alzheimer's disease model

BACKGROUND/OBJECTIVES

Alzheimer''s disease (AD) is characterized by deficits in memory and cognitive functions. The accumulation of amyloid beta peptide (Aβ) and oxidative stress in the brain are the most common causes of AD.

MATERIALS/METHODS

Caffeic acid (CA) is an active phenolic compound that has a variety of pharmacological actions. We studied the protective abilities of CA in an Aβ_25-35-injected AD mouse model. CA was administered at an oral dose of 10 or 50 mg/kg/day for 2 weeks. Behavioral tests including T-maze, object recognition, and Morris water maze were carried out to assess cognitive abilities. In addition, lipid peroxidation and nitric oxide (NO) production in the brain were measured to investigate the protective effect of CA in oxidative stress.

RESULTS

In the T-maze and object recognition tests, novel route awareness and novel object recognition were improved by oral administration of CA compared with the Aβ_25-35-injected control group. These results indicate that administration of CA improved spatial cognitive and memory functions. The Morris water maze test showed that memory function was enhanced by administration of CA. In addition, CA inhibited lipid peroxidation and NO formation in the liver, kidney, and brain compared with the Aβ_25-35-injected control group. In particular, CA 50 mg/kg/day showed the stronger protective effect from cognitive impairment than CA 10 mg/kg/day.

CONCLUSIONS

The present results suggest that CA improves Aβ_25-35-induced memory deficits and cognitive impairment through inhibition of lipid peroxidation and NO production.     

Correction: Highly sensitive and wearable gas sensors consisting of chemically functionalized graphene oxide assembled on cotton yarn

Correction for ‘Highly sensitive and wearable gas sensors consisting of chemically functionalized graphene oxide assembled on cotton yarn’ by Min-A. Kang et al., RSC Adv., 2018, 8, 11991–11996.

The authors regret that one of the funding bodies listed in the Acknowledgements section of the original article is incorrect. A revised version of the Acknowledgements section, in which ‘NRF-2016M3A7B4900119’ is replaced by ‘NRF-2017M3D9A1073502’, can be found below.This research was supported by a grant (2011-0031636) from the Center for Advanced Soft Electronics under the Global Frontier Research Program of the Ministry of Science, ICT and Future Planning, Korea. This research was also supported by Nano/Material Technology Development Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF-2017M3D9A1073502).The Royal Society of Chemistry apologises for these errors and any consequent inconvenience to authors and readers.     

Synthesis of silver sulfide nanoparticles and their photodetector applications

Silver sulfide nanoparticles (Ag₂S NPs) are currently being explored as infrared active nanomaterials that can provide environmentally stable alternatives to heavy metals such as lead. In this paper, we describe the novel synthesis of Ag₂S NPs by using a sonochemistry method and the fabrication of photodetector devices through the integration of Ag₂S NPs atop a graphene sheet. We have also synthesized Li-doped Ag₂S NPs that exhibited a significantly enhanced photodetector sensitivity via their enhanced absorption ability in the UV-NIR region. First-principles calculations based on a density functional theory formalism indicated that Li-doping produced a dramatic enhancement of NIR photoluminescence of the Ag₂S NPs. Finally, high-performance photodetectors based on CVD graphene and Ag₂S NPs were demonstrated and investigated; the hybrid photodetectors based on Ag₂S NPs and Li-doped Ag₂S NPs exhibited a photoresponse of 2723.2 and 4146.0 A W⁻¹ respectively under a light exposure of 0.89 mW cm⁻² at 550 nm. Our novel approach represents a promising and effective method for the synthesis of eco-friendly semiconducting NPs for photoelectric devices.

Silver sulfide nanoparticles (Ag₂S NPs) are currently being explored as infrared active nanomaterials that can provide environmentally stable alternatives to heavy metals such as lead.     

Interleukin-10 promoter polymorphisms in rheumatoid arthritis and Felty's syndrome

OBJECTIVE: To examine whether promoter polymorphisms associated with variation in interleukin-10 (IL-10) production are relevant to the development of rheumatoid arthritis (RA) or Felty's syndrome (FS). METHODS: DNA was obtained from 44 FS patients, 117 RA patients and 295 controls. The promoter region between -533 and - 1120 was amplified by polymerase chain reaction, and polymorphisms detected by restriction enzyme digest or sequence-specific oligonucleotide probing. RESULTS: We found no significant difference in allele or haplotype frequencies between the groups. CONCLUSION: There is no association between FS or RA and these recently identified IL-10 promoter polymorphisms. Other genetic or environmental factors could explain the alterations in IL-10 levels seen in these conditions.      

Analysis of PTEN Gene Mutations in Korean Patients With Cowden Syndrome and Polyposis Syndrome

PURPOSE PTEN (phosphatase and tensin homologue deleted in chromosome 10) is a candidate tumor suppressor gene. Mutations of this gene are responsible for PTEN hamartoma tumor syndromes, including Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus -like syndromes. Recently, PTEN mutations were identified in several human neoplasms. We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial adenomatous polyposis for germline or somatic PTEN mutations.METHODS The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial adenomatous polyposis. Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric polyps, colonic polyps, skin lesions, and peripheral blood mononuclear cells. To exclude common polymorphisms, 240 controls were tested.RESULTS All patients with Cowden syndrome showed several to numerous polyps in the gastrointestinal tract. A missense mutation at codon 217 (GTC to GAC, Val to Asp) in exon 7 was identified in one Cowden syndrome patient, and a nonsense mutation at codon 211 (TGC to TGA, Cys to stop) in exon 6 was identified in a second patient. Identical mutations were found in all tissue samples, including colonic polyps, from each patient. No PTEN mutations were found in their family members or in any patient with familial adenomatous polyposis. None of tested controls contained a mutation.CONCLUSIONS We have identified two new germline PTEN mutations in Korean patients with Cowden syndrome. Mutations in the introns and regulatory regions of the PTEN gene may be present in additional patients with Cowden syndrome and polyposis syndrome.Supported by a grant (Grant number 2003-261) from the Asan Institute for Life Sciences, Seoul, Korea.Reprints are not available.Presented at the meeting of International Gastrointestinal Bioregulation Conference, Hyogo, Japan, March 27, 2004.     

Ultra‐deep T cell receptor sequencing reveals the complexity and intratumour heterogeneity of T cell clones in renal cell carcinomas

The recognition of cancer cells by T cells can impact upon prognosis and be exploited for immunotherapeutic approaches. This recognition depends on the specific interaction between antigens displayed on the surface of cancer cells and the T cell receptor (TCR), which is generated by somatic rearrangements of TCR α‐ and β‐chains (TCRb). Our aim was to assess whether ultra‐deep sequencing of the rearranged TCRb in DNA extracted from unfractionated clear cell renal cell carcinoma (ccRCC) samples can provide insights into the clonality and heterogeneity of intratumoural T cells in ccRCCs, a tumour type that can display extensive genetic intratumour heterogeneity (ITH). For this purpose, DNA was extracted from two to four tumour regions from each of four primary ccRCCs and was analysed by ultra‐deep TCR sequencing. In parallel, tumour infiltration by CD4, CD8 and Foxp3 regulatory T cells was evaluated by immunohistochemistry and correlated with TCR‐sequencing data. A polyclonal T cell repertoire with 367–16 289 (median 2394) unique TCRb sequences was identified per tumour region. The frequencies of the 100 most abundant T cell clones/tumour were poorly correlated between most regions (Pearson correlation coefficient, –0.218 to 0.465). 3–93% of these T cell clones were not detectable across all regions. Thus, the clonal composition of T cell populations can be heterogeneous across different regions of the same ccRCC. T cell ITH was higher in tumours pretreated with an mTOR inhibitor, which could suggest that therapy can influence adaptive tumour immunity. These data show that ultra‐deep TCR‐sequencing technology can be applied directly to DNA extracted from unfractionated tumour samples, allowing novel insights into the clonality of T cell populations in cancers. These were polyclonal and displayed ITH in ccRCC. TCRb sequencing may shed light on mechanisms of cancer immunity and the efficacy of immunotherapy approaches. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Elevated Reactive Oxygen Species but not Glutathione Regulate Mercury Resistance to AML-2/DX100 Cells

The multidrug resistance-associated protein (MRP1) mediates cellular efflux of various xenobiotics and cellular resistance to heavy metals. Previously we reported that MRP1 mediates resistance to mercury exposure and possible mechanism mediating MRP1 expression after mercury exposure. This study was designed to investigate the role of reactive oxygen species (ROS) and glutathione on the resistance of AML-2/DX100 cells to mercuric chloride. The MRP1 overexpressing cells (AML-2/DX100) cells showed less scavenging activity to ROS induced by mercury while no difference in the basal glutathione levels between AML-2/WT and AML-2/DX100 cells. Mercury induced the activation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) but not c-jun-N-terminal kinase in AML-2/DX100 cells. The specific inhibitor for p38 MAPK and ERK, and antioxidant decreased the production of MRP1 and therefore resistance of AML-2/DX100 cells against mercury exposure. These results suggest that induction of ROS and downstream p38 MAPK and ERK were involved in the resistance of cells to mercury by expression MRP1 in AML-2/DX100 cells.