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The transcription of herpes simplex virus type 1 (HSV-1) genes is regulated by viral and cellular transcription factors and genome replication. One regulatory aspect is accessibility of viral genes to the host transcription machinery. In this study, we determine how the major HSV-1 transcriptional regulatory protein, ICP4, and viral DNA replication affect accessibility, and how this relates to viral gene transcription. We also assessed viral genome accessibility in a sensory neuronal model that has the potential for viral gene silencing and establishment of quiescent or latent infection. We conclude that the accessibility of the viral genome to the cellular machinery responsible for viral gene expression is an important determinant to infection outcome.

Main conclusion According to the results presented in this paper the fungal endophyte Epichloë typhina significantly improves the growth, PSII photochemistry and C assimilation efficiency of its host Dactylis glomerata. In this paper, we present a comprehensive study of the impact of the endophytic fungi Epichloë typhina on its plant hosts' photosynthesis apparatus. Chlorophyll a fluorescence, gas exchange, immuno-blotting and spectrophotometric measurements were employed to assess photosynthetic performance, changes in pigment content and mechanisms associated with light harvesting, carbon assimilation and energy distribution in Dactylis glomerata colonized with Epichloë typhina. According to the results presented in this study, colonization of D. glomerata results in improved photosynthesis efficiency. Additionally, we propose a new mechanism allowing plants to cope with the withdrawal of a significant fraction of its energy resources by the endophytic fungi. The abundance of LHCI, LHCII proteins as well as chlorophyll b was significantly higher in E+ plants. Malate export out of the chloroplast was shown to be increased in colonized plants. To our knowledge, we are the first to report this phenomenon. Epichloë colonization improved PSII photochemistry and C assimilation efficiency. Elevated energy demands of E+ D. glomerata plants are met by increasing the rate of carbon assimilation and PSII photochemistry.

Study design: Narrative review. Objectives: Review methods used to measure and classify obesity in individuals with spinal cord injuries (SCI). Outline the strengths and weaknesses of each method used to measure obesity in individuals with SCI. Setting: International. Methods: PubMed was used to identify articles before 2016. Search terms (‘obesity’ or ‘weight status’ and ‘spinal cord injury’). Filters: adults, English and human. Studies were retained that (1) included participants, 18 years or older, with SCI; (2) took place in inpatient, outpatient or community-based settings and (3) measured obesity status. Unique methods for classifying individuals with SCI as obese were identified and examples are presented. Results: Methods identified for classifying obesity were as follows: World Health Organization body mass index (BMI) cutoff⩾30 kg m −2 , BMI cutoff ⩾25-29 kg m −2 , and SCI-specific BMI cutoff ⩾22 kg m −2 , waist circumference cutoff (women >102 cm, men >88 cm), percent body fat cutoffs ⩾25% using bioelectrical impedance analysis and dual-energy X-ray absorptiometry, computerized tomography scan visceral fat area ⩾100 cm 2 and percentage of ideal body weight. Conclusions: BMI is the most widely used measure of obesity in the SCI literature. Although some studies identified alternative cutoffs or other metrics, there is no standardized obesity classification in SCI. However, research is needed to determine and validate obesity classification specific to SCI due to physiological changes that occur following injury. We recommend that researchers and clinicians proceed with caution and use methodology based on the purpose of measurement.

The ability of skeletal muscle to enhance lipid utilization during exercise is a form of metabolic plasticity essential for survival. Conversely, metabolic inflexibility in muscle can cause organ dysfunction and disease. Although the transcription factor Kruppel-like factor 15 (KLF15) is an important regulator of glucose and amino acid metabolism, its endogenous role in lipid homeostasis and muscle physiology is unknown. Here we demonstrate that KLF15 is essential for skeletal muscle lipid utilization and physiologic performance. KLF15 directly regulates a broad transcriptional program spanning all major segments of the lipid-flux pathway in muscle. Consequently, Klf15-deficient mice have abnormal lipid and energy flux, excessive reliance on carbohydrate fuels, exaggerated muscle fatigue, and impaired endurance exercise capacity. Elucidation of this heretofore unrecognized role for KLF15 now implicates this factor as a central component of the transcriptional circuitry that coordinates physiologic flux of all three basic cellular nutrients: glucose, amino acids, and lipids.

Mutations in the MIP phosphatase MTMR14 are associated with human autosomal centronuclear myopathy. Mice that lack MIP have impaired muscle performance and enhanced fatigue due to the accumulation of MIP substrates PtdIns(3,5)P2 and PtdIns(3,4)P2, which cause alterations in intracellular Ca2+ levels. The intracellular Ca 2+ concentration ([Ca 2+ ] i ) in skeletal muscles must be rapidly regulated during the excitation-contraction-relaxation process 1 . However, the signalling components involved in such rapid Ca 2+ movement are not fully understood. Here we report that mice deficient in the newly identified PtdInsP (phosphatidylinositol phosphate) phosphatase MIP/MTMR14 (muscle-specific inositol phosphatase) show muscle weakness and fatigue. Muscles isolated from MIP/MTMR14 −/− mice produced less contractile force, had markedly prolonged relaxation and showed exacerbated fatigue relative to normal muscles. Further analyses revealed that MIP/MTMR14 deficiency resulted in spontaneous Ca 2+ leakage from the internal store — the sarcoplasmic reticulum. This was attributed to decreased metabolism (dephosphorylation) and the subsequent accumulation of MIP/MTMR14 substrates, especially PtdIns(3,5)P 2 and PtdIns (3,4)P 2 . Furthermore, we found that PtdIns(3,5)P 2 and PtdIns(3,4)P 2 bound to, and directly activated, the Ca 2+ release channel (ryanodine receptor 1, RyR1) of the sarcoplasmic reticulum. These studies provide the first evidence that finely controlled PtdInsP levels in muscle cells are essential for maintaining Ca 2+ homeostasis and muscle performance.

Conditions such as respiratory failure and cardiopulmonary arrest can expose the diaphragm to hypoxemia. In skeletal muscles, fatiguing stimulation renders muscles hypoxic, which has long been known to dramatically reduce muscle function. We have previously demonstrated that fatiguing stimulation under hypoxic conditions disrupts both the excitation-contraction coupling (ECC) process and the isometric contractile properties (ICP) in intact diaphragm muscle strips and the contractile properties of skinned fibers isolated from these muscles. Here we have analyzed the effects of intermittent fatiguing stimulation on specific muscle proteins in muscle strips from mouse diaphragms that have been exposed to hypoxia. We report for the first time that the effects of hypoxia-fatigue, namely to decrease maximal tetanic force, maximal calcium-activated force and calcium sensitivity of the mouse diaphragm muscle, are associated with the degradation of troponins TnI and TnC (Western blot analysis). The concentrations of TnT and actin did not change under these same conditions. Because troponins are integrally involved in regulating the interaction between actin and myosin during the cross-bridge cycle, the degradation of TnI and TnC may explain the effects of hypoxia-fatigue on the ICP. This interpretation is supported by the observations that extraction of troponins from control skinned fibers mimics the effects of hypoxia-fatigue on contractile function and that incorporation of native troponins into fibers isolated from hypoxic-fatigued muscles partially restores function.

Changes in malate concentration and activity of NADP-dependent malic enzyme were observed as the effect of Botrytis cinerea infection of C 3 or CAM-performing Mesembryanthemum crystallinum p lants. Biotic stress applied on C 3 plants led to increase in malate concentration during the night and in consequence it led to increase in Δ-malate (day/night fluctuations) in infected leaves on the 2nd day post infection (dpi). It corresponded with induction of additional isoform of NADP-malic enzyme (NADP-ME3). On the contrary, CAM-performing M. crystallinum plants exhibited decrease in malate concentration and decay in its diurnal fluctuations as a reaction to B. cinerea infection. This correlated with significant decrease in activities of NADP-malic enzyme isoforms on the 2nd dpi as well as no fluctuations in their activities on the 9th dpi. Presented results point out to differences between C 3 and CAM plants in the direction of changes in primary metabolism providing energy, reducing equivalents and carbon skeletons for defense responses to halt the pathogen growth.

The intracellular Ca(2+) concentration ([Ca(2+)](i)) in skeletal muscles must be rapidly regulated during the excitation-contraction-relaxation process. However, the signalling components involved in such rapid Ca(2+) movement are not fully understood. Here we report that mice deficient in the newly identified PtdInsP (phosphatidylinositol phosphate) phosphatase MIP/MTMR14 (muscle-specific inositol phosphatase) show muscle weakness and fatigue. Muscles isolated from MIP/MTMR14(-/-) mice produced less contractile force, had markedly prolonged relaxation and showed exacerbated fatigue relative to normal muscles. Further analyses revealed that MIP/MTMR14 deficiency resulted in spontaneous Ca(2+) leakage from the internal store - the sarcoplasmic reticulum. This was attributed to decreased metabolism (dephosphorylation) and the subsequent accumulation of MIP/MTMR14 substrates, especially PtdIns(3,5)P(2) and PtdIns (3,4)P(2). Furthermore, we found that PtdIns(3,5)P(2) and PtdIns(3,4)P(2) bound to, and directly activated, the Ca(2+) release channel (ryanodine receptor 1, RyR1) of the sarcoplasmic reticulum. These studies provide the first evidence that finely controlled PtdInsP levels in muscle cells are essential for maintaining Ca(2+) homeostasis and muscle performance.

The final report of the National Study on Women with Disabilities provides an overview of the research conducted from 1992 to 1996 at the Center for Research on Women with Disabilities. The report addresses the methodologies used in the recruitment of women and reviews the various analyses conducted on the data. In addition, the report provides a discussion of recruitment techniques used for nondisabled women and the analysis used for this population as well. It provides a summary of findings in the areas of sense of self, relationships, information about sexuality, sexual functioning, pregnancy, sexually transmitted diseases, abuse, chronic conditions, health maintenance behaviors, gynecologic health, and health care utilization.

Fatigue studies of isolated, intact muscles typically utilize solutions saturated with O2. However, under in vivo fatiguing conditions, less oxygen is delivered to the muscles and they actually experience hypoxia. No studies to date have correlated the effects of acute hypoxia on the isometric contractile properties of intact muscles, skinned fibers isolated from the same muscles, and the cellular content of specific muscle proteins. Therefore, we have studied the effects of in vitro acute hypoxia on the fatigability of intact diaphragm muscle strips and on the isometric contractile properties of single Triton-skinned fibers isolated from control and hypoxic diaphragm muscles. We found that hypoxia and fatiguing stimulation per se affect the tetanic force of intact muscle strips without exhibiting any significant deleterious effects on the calcium-activated force of skinned muscle fibers dissected from the intact muscles. In contrast, fatiguing stimulation under hypoxic conditions decreased both the tetanic force of muscle strips and the calcium-activated force of skinned muscle fibers. Gel electrophoresis of muscles subjected to hypoxia and hypoxic-fatigue revealed that there is a significant reduction in three protein bands when compared to control muscles. Protein modification may be the underlying mechanism of muscle fatigue under physiologic conditions.