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Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.Objectives Magnetic resonance imaging (MRI) is a cornerstone in diagnosis of myopathies. The present study sought to elucidate possible associations between electromyography (EMG) findings and histogram parameters derived from clinical MRI in myositis and other myopathies. Materials and methods Twenty six patients with myopathies were included in this retrospective study. Clinical MRI was performed with a 1.5T MRI scanner including T2- and T1-weighted images. EMG analysis was performed during clinical diagnostic workup. The histogram parameters of the MRI sequences were obtained of the same muscle, which was investigated with EMG. Results Several correlations were identified between mean duration of the motor unit potentials (MUP) and histogram parameters derived from T1- and T2-weighted images. The highest for T1-weighted images was mode (r = -.73, P less then .0001) and for T2-weighted images was p25 (r = -.57, P = .022). There were significant differences for several histogram parameters between muscles with pathological spontaneous activity and without. So, for T1-weighted images, the best discrimination was achieved with mean (P = .096), and for T2-weighted images for p10 (P = .05). Mean SI values derived from T1-weighted images achieved an AUC of 0.84 with a sensitivity of 0.81 and a specificity of 0.86 to discriminate patients with and without pathological spontaneous activity (PSA). Conclusions The present study identified strong associations between histogram analysis derived from morphological MRI sequences and the duration of the MUP derived from EMG in myopathies strengthening the fact that both diagnostic modalities can reflect disease state in a similar fashion. Histogram parameters can predict muscles with PSA.Objective The aim of this paper was to explore child sexually abused survivors' experiences of dental treatment in order to obtain a deeper understanding of them as dental patients. Methods Data were drawn from qualitative semi-structured interviews with 16 adult informants recruited from four different Centres against Sexual Abuse in Norway. Data analysis was developed according to the principles of grounded theory suggested by Charmaz. Results A conceptual framework was generated, and a core concept was constructed from the informants' reports of their experiences of dental treatment Preparing for attack and recovering from battle based on four main categories (a) Expecting danger, (b) Battling anxiety, (c) Reliving abuse and (d) Struggling with the aftermath. Conclusions The analyses increase the understanding of how child sexual abuse survivors prepare before-battle during-and recover after dental treatment. This study revealed child sexual abuse survivors' experiences of extensive anxiety, triggered by sensory stimuli such as sensations, movement, muscles, touch, sight, sound, smell and taste, associated with dental procedures per se, but also sensory stimuli similar to previous traumatic experiences. The findings suggest that child sexual abuse survivors' dental anxiety is primarily trauma-driven and possibly being one of the long-term effects of child sexual abuse. This may be an important contribution to the understanding of CSA survivors and should affect the approach of clinicians treating dental patients with such a history.Background and purpose The sites and actions of ethanol in the central nervous system have been studied for many years, yet the precise mechanisms for its actions are not well understood. For example, like other drugs of abuse, it affects dopamine levels in the nucleus accumbens (nAc), an important region of the mesolimbic system, causing a reinforcing effect. Previous studies have shown that glycine receptors (GlyRs) present in the nAc are potentiated by clinically-relevant concentrations of ethanol, where α1 and α2 are the predominant subunits expressed. Experimental approach Using a combination of electrophysiology and behavioral assays, we studied the involvement of GlyR α2 subunits on the effects of low and high doses of ethanol, as well as in consumption using mice lacking GlyR α2 subunits (male Glra2-/Y and female Glra2-/- ). Key results Our results support the existence of GlyR α2 subunits in accumbal neurons, since the glycine-evoked currents and glycinergic mIPSCs in the Glra2-/Y mice were drastically decreased. Regarding ethanol effects, we found differences in behavioral studies for ethanol consumption and sedation between WT and Glra2 knockout mice. For example, using the drinking in the dark (DID) paradigm, we found that Glra2-/Y mice presented a binge-like drinking behavior immediately when exposed to ethanol and not a gradual consumption like wild-type animals. Interestingly, the effect of knocking out the Glra2 gene in female (Glra2-/- ) mice was less evident, since wild-type female mice already showed higher DID. Conclusion and implications The differences in ethanol consumption between WT and KO mice provide additional evidence supporting the conclusion that GlyRs are biologically-relevant targets for sedative and rewarding properties of ethanol.Background and purpose Volatile anesthetics have been shown to differentially modulate mammalian Shaker-related voltage-gated potassium (Kv1) channels. This study was designed to investigate molecular and cellular mechanisms underlying the modulatory effects of desflurane or sevoflurane on the human Kv1.5 (hKv1.5) channel. Experimental approach Thirteen single-point mutations were constructed within pore domain of hKv1.5 channel using site-directed mutagenesis. The effects of desflurane or sevoflurane on heterologously expressed wild-type and mutant hKv1.5 channels were examined by whole-cell patch-clamp technique. A computer simulation was conducted to predict the docking pose of desflurane or sevoflurane within hKv1.5 channel. Olaparib Key results Both desflurane and sevoflurane increased hKv1.5 current at mild depolarizations but decreased it at strong depolarizations, indicating that these anesthetics produce both stimulatory and inhibitory actions on hKv1.5 channel. The inhibitory effect of desflurane or sevoflurane on hKv1.
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