Effects of anger and anger regulation styles on pain in daily life of women with fibromyalgia: A diary study

BackgroundFibromyalgia is characterized by an amplified pain response to various physical stimuli. Through biological and behavioural mechanisms, patients with fibromyalgia may also show an increase of pain in response to emotions. Anger, and how it is regulated, may be particularly important in chronic pain.AimTo examine, among patients with fibromyalgia, whether anger during everyday life amplifies pain and whether general and situational anger inhibition and anger expression modulate the anger–pain link.MethodsFor 28 consecutive days, 333 women with fibromyalgia (mean age 47 ± 12 years) reported their transient anger and state anger inhibition (anger-in) and expression (anger-out) responses regarding a significant emotional event during the day as well as end-of-day pain. Trait anger inhibition and expression were assessed by questionnaire. Multilevel regression analyses were performed.ResultsState anger predicted higher end-of-day pain (p < .001) in half of the patients, but lower pain in one-quarter of patients. State anger inhibition was unrelated to pain. Trait anger inhibition was related to more pain (p = .02). The lowest pain level was observed among patients with high trait anger expression who actually expressed their anger in an anger-arousing situation (p = .02).ConclusionsOur study suggests that anger and a general tendency to inhibit anger predicts heightened pain in the everyday life of female patients with fibromyalgia. Psychological intervention could focus on healthy anger expression to try to mitigate the symptoms of fibromyalgia.     

Proteomic analysis of alternative protein tyrosine phosphorylation in 1,2-dichlorovinyl-cysteine-induced cytotoxicity in primary cultured rat renal proximal tubular cells

Toxicant exposure affects the activity of various protein tyrosine kinases. Using phosphotyrosine proteomics, we identified proteins that were differentially phosphorylated before renal cell detachment and apoptosis. Treatment of primary cultured rat proximal tubular epithelial cells with the model nephrotoxicant S-(1,2-dichlorovinyl)-L-cysteine (DCVC) resulted in early reorganization of F-actin stress fibers and formation of lamellipodia, which was followed by cell detachment from the matrix and apoptosis. This was prevented by genistein-mediated inhibition of protein tyrosine kinases and enhanced by inhibition of protein tyrosine phosphatases using vanadate. Phosphotyrosine proteomics revealed that DCVC-induced renal cell apoptosis was preceded by changes in the tyrosine phosphorylation status of a subset of proteins, as identified by matrix-assisted laser desorption ionization/time of flight-mass spectrometry (MS)/MS including actin-related protein 2 (Arp2), cytokeratin 8, t-complex protein 1 (TCP-1), chaperone containing TCP-1, and gelsolin precursor. The major differentially tyrosine-phosphorylated protein was Arp2, whereas phosphorylation of Arp3 was not affected. Arp2 was located in the lamellipodia that were formed before the onset of apoptosis. Because DCVC-induced cell detachment and apoptosis is regulated by tyrosine kinases, we propose that alterations in tyrosine phosphorylation of a subset of proteins, including Arp2, play a role in the regulation of the F-actin reorganization and lamellipodia formation that precede renal cell apoptosis caused by nephrotoxicants.     

Diagnostic and prognostic accuracy of clinical and laboratory parameters in community-acquired pneumonia

Background  

Community-acquired pneumonia (CAP) is the most frequent infection-related cause of death. The reference standard to diagnose CAP is a new infiltrate on chest radiograph in the presence of recently acquired respiratory signs and symptoms. This study aims to evaluate the diagnostic and prognostic accuracy of clinical signs and symptoms and laboratory biomarkers for CAP.     

MR‐based measurements and simulations of the magnetic field created by a realistic transcranial magnetic stimulation (TMS) coil and stimulator

Transcranial magnetic stimulation (TMS) is an emerging technique that allows non‐invasive neurostimulation. However, the correct validation of electromagnetic models of typical TMS coils and the correct assessment of the incident TMS field (B_TMS) produced by standard TMS stimulators are still lacking. Such a validation can be performed by mapping B_TMS produced by a realistic TMS setup. In this study, we show that MRI can provide precise quantification of the magnetic field produced by a realistic TMS coil and a clinically used TMS stimulator in the region in which neurostimulation occurs. Measurements of the phase accumulation created by TMS pulses applied during a tailored MR sequence were performed in a phantom. Dedicated hardware was developed to synchronize a typical, clinically used, TMS setup with a 3‐T MR scanner. For comparison purposes, electromagnetic simulations of B_TMS were performed. MR‐based measurements allow the mapping and quantification of B_TMS starting 2.5 cm from the TMS coil. For closer regions, the intra‐voxel dephasing induced by B_TMS prohibits TMS field measurements. For 1% TMS output, the maximum measured value was ~0.1 mT. Simulations reflect quantitatively the experimental data. These measurements can be used to validate electromagnetic models of TMS coils, to guide TMS coil positioning, and for dosimetry and quality assessment of concurrent TMS‐MRI studies without the need for crude methods, such as motor threshold, for stimulation dose determination.     

19 F MRSI of capecitabine in the liver at 7 T using broadband transmit–receive antennas and dual‐band RF pulses

Capecitabine (Cap) is an often prescribed chemotherapeutic agent, successfully used to cure some patients from cancer or reduce tumor burden for palliative care. However, the efficacy of the drug is limited, it is not known in advance who will respond to the drug and it can come with severe toxicity. ¹⁹ F Magnetic Resonance Spectroscopy (MRS) and Magnetic Resonance Spectroscopic Imaging (MRSI) have been used to non‐invasively study Cap metabolism in vivo to find a marker for personalized treatment. In vivo detection, however, is hampered by low concentrations and the use of radiofrequency (RF) surface coils limiting spatial coverage. In this work, the use of a 7T MR system with radiative multi‐channel transmit–receive antennas was investigated with the aim of maximizing the sensitivity and spatial coverage of ¹⁹ F detection protocols. The antennas were broadband optimized to facilitate both the ¹H (298 MHz) and ¹⁹ F (280 MHz) frequencies for accurate shimming, imaging and signal combination. B₁⁺ simulations, phantom and noise measurements showed that more than 90% of the theoretical maximum sensitivity could be obtained when using B₁⁺ and B₁^? information provided at the ¹H frequency for the optimization of B₁⁺ and B₁^? at the ¹⁹ F frequency. Furthermore, to overcome the limits in maximum available RF power, whilst ensuring simultaneous excitation of all detectable conversion products of Cap, a dual‐band RF pulse was designed and evaluated. Finally, ¹⁹ F MRS(I) measurements were performed to detect ¹⁹ F metabolites in vitro and in vivo. In two patients, at 10 h (patient 1) and 1 h (patient 2) after Cap intake, ¹⁹ F metabolites were detected in the liver and the surrounding organs, illustrating the potential of the set‐up for in vivo detection of metabolic rates and drug distribution in the body. Copyright © 2015 John Wiley & Sons, Ltd.     

On the transmit field inhomogeneity correction of relaxation‐compensated amide and NOE CEST effects at 7 T

High field MRI is beneficial for chemical exchange saturation transfer (CEST) in terms of high SNR, CNR, and chemical shift dispersion. These advantages may, however, be counter‐balanced by the increased transmit field inhomogeneity normally associated with high field MRI. The relatively high sensitivity of the CEST contrast to B₁ inhomogeneity necessitates the development of correction methods, which is essential for the clinical translation of CEST. In this work, two B₁ correction algorithms for the most studied CEST effects, amide‐CEST and nuclear Overhauser enhancement (NOE), were analyzed. Both methods rely on fitting the multi‐pool Bloch‐McConnell equations to the densely sampled CEST spectra. In the first method, the correction is achieved by using a linear B₁ correction of the calculated amide and NOE CEST effects. The second method uses the Bloch‐McConnell fit parameters and the desired B₁ amplitude to recalculate the CEST spectra, followed by the calculation of B₁‐corrected amide and NOE CEST effects. Both algorithms were systematically studied in Bloch‐McConnell equations and in human data, and compared with the earlier proposed ideal interpolation‐based B₁ correction method. In the low B₁ regime of 0.15–0.50 μT (average power), a simple linear model was sufficient to mitigate B₁ inhomogeneity effects on a par with the interpolation B₁ correction, as demonstrated by a reduced correlation of the CEST contrast with B₁ in both the simulations and the experiments.     

No association between two MLH3 variants (S845G and P844L)and colorectal cancer risk

Recently we identified a new variant, S845G, in the MLH3 gene in 7 out of 327 patients suspected of hereditary nonpolyposis colorectal cancer but not fulfilling the Amsterdam criteria and in 1 out of 188 control subjects. As this variant might play a role in causing sporadic colorectal cancer, we analyzed its prevalence in sporadic colorectal cancer patients. We analyzed a small part of exon 1 of the MLH3 gene, including the S845G variant, in germline DNA of 467 white sporadic colorectal cancer patients and 497 white controls. The S845G variant was detected in five patients and eight controls; the results thus indicate that this variant does not confer an increased colorectal cancer risk. Another variant (P844L) was clearly a polymorphism. Three other missense variants were rare and the sample size of the study was too small to conclude whether they are pathogenic. In conclusion, no association was observed between two MLH3 variants (P844L and S845G) and colorectal cancer risk.