Neurovirulent strains of herpes simplex virus type 1 are not necessarily competent for reactivatable latency.

Ability of two neurovirulent strains (F and +GC (LPV) Miyama) of herpes simplex virus type 1 (HSV-1) to establish and maintain reactivatable latency in trigeminal ganglia (TG) was compared after intranasal inoculation of mice. The +GC (LPV) Miyama strain showed a very low rate of virus reactivation in explant cultures of TG, while the F strain showed a high rate of reactivation. These data indicate that neurovirulent strains of HSV-1 are not always competent for reactivatable latency, although most virulent strains of HSV-1 thus far reported were competent for reactivatable latency.&#60;/P&#62;</p

Reactivatable latency of three avirulent strains of herpes simplex virus type 1 after intranasal inoculation in mice.

In order to elucidate the mechanism of latent infection of herpes simplex virus (HSV), reactivatable latency of three avirulent strains (SKO-1B, -GCr Miyama, SKa) of HSV type 1 was comparatively examined in a mouse latency model. The SKO-1B strain showed high rate of virus reactivation from explanted trigeminal ganglia without n-butyrate enhancement, while the other two strains showed a very low rate of virus reactivation in the absence of n-butyrate. In the presence of n-butyrate, however, the rate of the -GCr Miyama strain jumped to a comparable level with that of SKO-1B, although the rate of SKa remained at a low level. A more precise follow-up experiment changing the virus dose highlighted the difference of the ability to reactivate from the latent state between SKO-1B and -GCr Miyama. Virus titer in trigeminal ganglia during acute phase, infectivity to cell lines of neural origin, and susceptibility to acyclovir and phosphonoacetate were assayed to know the reasons for the variation in the ability of reactivatable latency among these strains. It was concluded that the reduced infectivity to neural cells, and limited ability of reactivatable latency shown by the SKa strain could mainly be attributed to the deficiency of thymidine kinase activity.&#60;/P&#62;</p

Is there evidence for the asymmetrical transfer of strength to an untrained limb?

Purpose: The literature predominantly addresses cross-education of strength in the dominant limb rather than the non-dominant limb, guided by the hypothesis of an asymmetrical transfer of strength from unilateral training protocols. The purpose of the study was to review the literature and determine how much evidence was available to support this claim. A meta-analysis was performed to estimate the magnitude of this hypothesized asymmetrical transfer of strength. Methods: A literature search of all possible records was implemented using Cochrane Library, PubMed, and Scopus from February 2022 to May 2022. Comparison of randomized controlled trials was computed. The change scores and standard deviations of those change scores were extracted for each group. Only three studies met the criteria, from which a total of five effect sizes were extracted and further analyzed. Results: The overall effect of resistance training of the dominant limb on strength transfer to the non-dominant limb relative to the effects of resistance training the non-dominant limb on strength transfer to the dominant (non-training) limb was 0.46 (SE 0.42). The analysis from this study resulted in minimal support for the asymmetry hypothesis. Given the small number of studies available, we provide the effect but note that the estimate is unlikely to be stable. Conclusion: Although it is repeatedly stated that there is an asymmetrical transfer of strength, our results find little support for that claim. This is not to say that it does not exist, but additional research implementing a control group and a direct comparison between limbs is needed to better understand this question

Resting-state functional connectivity-based biomarkers and functional MRI-based neurofeedback for psychiatric disorders: a challenge for developing theranostic biomarkers

Psychiatric research has been hampered by an explanatory gap between psychiatric symptoms and their neural underpinnings, which has resulted in poor treatment outcomes. This situation has prompted us to shift from symptom-based diagnosis to data-driven diagnosis, aiming to redefine psychiatric disorders as disorders of neural circuitry. Promising candidates for data-driven diagnosis include resting-state functional connectivity MRI (rs-fcMRI)-based biomarkers. Although biomarkers have been developed with the aim of diagnosing patients and predicting the efficacy of therapy, the focus has shifted to the identification of biomarkers that represent therapeutic targets, which would allow for more personalized treatment approaches. This type of biomarker (i.e., theranostic biomarker) is expected to elucidate the disease mechanism of psychiatric conditions and to offer an individualized neural circuit-based therapeutic target based on the neural cause of a condition. To this end, researchers have developed rs-fcMRI-based biomarkers and investigated a causal relationship between potential biomarkers and disease-specific behavior using functional MRI (fMRI)-based neurofeedback on functional connectivity. In this review, we introduce recent approach for creating a theranostic biomarker, which consists mainly of two parts: (i) developing an rs-fcMRI-based biomarker that can predict diagnosis and/or symptoms with high accuracy, and (ii) the introduction of a proof-of-concept study investigating the relationship between normalizing the biomarker and symptom changes using fMRI-based neurofeedback. In parallel with the introduction of recent studies, we review rs-fcMRI-based biomarker and fMRI-based neurofeedback, focusing on the technological improvements and limitations associated with clinical use.Comment: 46 pages, 5 figure

A practical method for assessing lip compression strengthening in healthy adults

© 2020 by the authors. There is no practical and accessible assessment method to evaluate lip muscle compression strength. The purpose of this study was to examine the relationship between the standard method (i.e., Iowa Oral Performance Instrument) and a practical method in healthy adults. In order to achieve our research purpose, ninety-eight healthy adults (18-40 years) completed lip compression strength measurements (standard method) and lip grasping performance tests using a standard recyclable plastic water bottle (practical method). In the overall sample, the mean and standard deviation for standard method and practical method was 26.7 (7.0) kPa and 255 (119) g, respectively. For the overall sample (n = 98), there was a positive relationship between the two strength tasks [r = 0.56 (0.41, 0.68)]. When separated by sex, positive correlations were observed for men and women with no differences between the observed correlations [difference of 0.06 (-0.2646, 0.3917)]. This result indicates that those individuals who are strong in the standard task will often be strong in the practical task. Future research is needed to determine how well changes in each test track with each other in response to a lip strength training program

Assessments of facial muscle thickness by ultrasound in younger adults: Absolute and relative reliability

© 2019 by the authors. The absolute reliability (i.e., standard error of measurement and minimal difference) of a measurement is important to consider when assessing training effects. However, the absolute reliability for ultrasound measured facial muscle thickness had not been investigated. In order to examine the absolute and relative reliability of measuring facial muscles, 98 healthy, young, and middle-aged adults (18-40 years) had ultrasound measurements taken twice, separated by an average of three days. Six facial muscles were selected to determine the reliability of facial muscle thickness. The relative reliability (ICC3,1) ranged from 0.425 for the orbicularis oris (inferior) to 0.943 for the frontalis muscle. The absolute reliability (minimal difference) ranged from 0.25 mm for the orbicularis oculi to 1.82 mm for the masseter. The percentage minimal difference was 22%, 25%, 26%, 29%, 21%, and 10% for the frontalis, orbicularis oculi, orbicularis oris (superior), orbicularis oris (inferior), depressor anguli oris, and masseter, respectively. Our results indicated that the relative reliability was similar to that observed previously. The absolute reliability indicated that the measurement error associated with measuring muscle thickness of the face may be greater than that of the trunk/limb muscles. This may be related to the difficulty of accurately determining the borders of each muscle

Cluster II che genes of Pseudomonas syringae pv. tabaci 6605, orthologs of cluster I in Pseudomonas aeruginosa, are required for chemotaxis and virulence

Pseudomonas syringae pv. tabaci 6605 (Pta6605) is a causal agent of wildfire disease in host tobacco plants and is highly motile. Pta6605 has multiple clusters of chemotaxis genes including cheA, a gene encoding a histidine kinase, cheY, a gene encoding a response regulator, mcp, a gene for a methyl-accepting chemotaxis protein, as well as flagellar and pili biogenesis genes. However, only two major chemotaxis gene clusters, cluster I and cluster II, possess cheA and cheY. Deletion mutants of cheA or cheY were constructed to evaluate their possible role in Pta6605 chemotaxis and virulence. Motility tests and a chemotaxis assay to known attractant demonstrated that cheA2 and cheY2 mutants were unable to swarm and to perform chemotaxis, whereas cheA1 and cheY1 mutants retained chemotaxis ability almost equal to that of the wild-type (WT) strain. Although WT and cheY1 mutants of Pta6605 caused severe disease symptoms on host tobacco leaves, the cheA2 and cheY2 mutants did not, and symptom development with cheA1 depended on the inoculation method. These results indicate that chemotaxis genes located in cluster II are required for optimal chemotaxis and host plant infection by Pta6605 and that cluster I may partially contribute to these phenotypes

Systems Analysis of ATF3 in Stress Response and Cancer Reveals Opposing Effects on Pro-Apoptotic Genes in p53 Pathway

Stress-inducible transcription factors play a pivotal role in cellular adaptation to environment to maintain homeostasis and integrity of the genome. Activating transcription factor 3 (ATF3) is induced by a variety of stress and inflammatory conditions and is over-expressed in many kinds of cancer cells. However, molecular mechanisms underlying pleiotropic functions of ATF3 have remained elusive. Here we employed systems analysis to identify genome-wide targets of ATF3 that is either induced by an alkylating agent methyl methanesulfonate (MMS) or over-expressed in a prostate tumour cell line LNCaP. We show that stress-induced and cancer-associated ATF3 is recruited to 5,984 and 1,423 targets, respectively, in the human genome, 89% of which are common. Notably, ATF3 targets are highly enriched for not only ATF/CRE motifs but also binding sites of several other stress-inducible transcription factors indicating an extensive network of stress response factors in transcriptional regulation of target genes. Further analysis of effects of ATF3 knockdown on these targets revealed that stress-induced ATF3 regulates genes in metabolic pathways, cell cycle, apoptosis, cell adhesion, and signalling including insulin, p53, Wnt, and VEGF pathways. Cancer-associated ATF3 is involved in regulation of distinct sets of genes in processes such as calcium signalling, Wnt, p53 and diabetes pathways. Notably, stress-induced ATF3 binds to 40% of p53 targets and activates pro-apoptotic genes such as TNFRSF10B/DR5 and BBC3/PUMA. Cancer-associated ATF3, by contrast, represses these pro-apoptotic genes in addition to CDKN1A/p21. Taken together, our data reveal an extensive network of stress-inducible transcription factors and demonstrate that ATF3 has opposing, cell context-dependent effects on p53 target genes in DNA damage response and cancer development