RESUMEN

Despite residual functional deficits clinically observed in conservatively treated mid-shaft clavicle fractures, no study has reported a quantitative assessment of the treatment effects on the kinematics of the shoulder complex during functional movement. Using computerised motion analysis, the current study quantified the 3D residual kinematic deviations or strategies of the shoulder complex bones during multi-plane elevations in fifteen patients with conservatively treated mid-shaft clavicle fractures and fifteen healthy controls. Despite residual clavicular malunion, the patients recovered normal shoulder kinematics for arm elevations up to 60° in all three tested planes. For elevations beyond 60°, normal clavicle kinematics but significantly increased scapular posterior tilt relative to the trunk was observed in the patient group, leading to significantly increased clavicular protraction and posterior tilt relative to the scapula (i.e., AC joint). Slightly different changes were found in the sagittal plane, showing additional changes of increased scapular upward rotations at 90° and 120° elevations. Similar kinematic changes were also found on the unaffected side, indicating a trend of symmetrical bilateral adaptation. The current results suggest that shoulder kinematics in multi-plane arm elevations should be monitored for any compromised integrated motions of the individual bones following conservative treatment. Rehabilitation strategies, including muscle strengthening and synergy stability training, should also consider compensatory kinematic changes on the unaffected side to improve the bilateral movement control of the shoulder complex during humeral elevation.

RESUMEN

Purpose: To characterize inner retinal microvasculature of rhesus monkeys with a range of refractive errors using optical coherence tomography angiography. Method: Refractive error was induced in right eyes of 18 rhesus monkeys. At 327 to 347 days of age, axial length and spherical equivalent refraction (SER) were measured, and optical coherence tomography and optical coherence tomography angiography scans (Spectralis, Heidelberg) were collected. Magnification-corrected metrics included foveal avascular zone area and perfusion density, fractal dimension, and lacunarity of the superficial vascular complex (SVC) and deep vascular complex (DVC) in the central 1-mm diameter and 1.0- to 1.5-mm, 1.5- to 2.0-mm, and 2.0- to 2.5-mm annuli. Pearson correlations were used to explore relationships. Results: The mean SER and axial length were 0.78 ± 4.02 D (-7.12 to +7.13 D) and 17.96 ± 1.08 mm (16.41 to 19.93 mm), respectively. The foveal avascular zone area and SVC perfusion density were correlated with retinal thickness for the central 1 mm (P < 0.05). SVC perfusion density of 2.0- to 2.5-mm annulus decreased with increasing axial length (P < 0.001). SVC and DVC fractal dimensions of 2.0- to 2.5-mm were correlated with axial length and SER, and DVC lacunarity of 1.5- to 2.0-mm annulus was correlated with axial length (P < 0.05). Conclusions: Several inner retinal microvasculature parameters were associated with increasing axial length and SER in juvenile rhesus monkeys. These findings suggest that changes in retinal microvasculature could be indicators of refractive error development. Translational Relevance: In juvenile rhesus monkeys, increasing myopic refraction and axial length are associated with alterations in the inner retinal microvasculature, which may have implications in myopia-related changes in humans.

Asunto(s)

Macaca mulatta , Microvasos , Refracción Ocular , Vasos Retinianos , Tomografía de Coherencia Óptica , Animales , Tomografía de Coherencia Óptica/métodos , Vasos Retinianos/diagnóstico por imagen , Microvasos/diagnóstico por imagen , Refracción Ocular/fisiología , Modelos Animales de Enfermedad , Errores de Refracción/fisiopatología , Errores de Refracción/patología , Angiografía con Fluoresceína/métodos , Masculino , Longitud Axial del Ojo/diagnóstico por imagen , Femenino

RESUMEN

Purpose: The purpose of this study was to determine the effects of axial elongation on optic nerve head morphology and macula inner retinal thickness in young rhesus monkeys. Methods: Both eyes of 26 anisometropic, 1-year-old rhesus monkeys were imaged using optical coherence tomography (OCT). Before imaging, the animals were sedated, their eyes were dilated, and axial length was measured using an optical biometer. OCT imaging included a 20 degrees, 24-line radial scan centered on the optic nerve head (ONH) and two 20 degrees × 20 degrees raster scans, one centered on the ONH and the other on the macula. Radial scans were analyzed using programs written in MATLAB to quantify the Bruch's membrane opening (BMO) area and position, minimum rim width (MRW), anterior lamina cribrosa surface (ALCS) position, size of any scleral crescent, circumpapillary retinal nerve fiber layer (RNFL), and choroid thickness (pCh). Macula total retinal thickness (mTRT) and ganglion cell inner plexiform layer (GCIPL) thicknesses were quantified from macula scans. Linear least square regression was determined for OCT measures and axial length of the right eye, and for inter-eye differences. Results: Animals were 341 ± 18 days old at the time of imaging. BMO area (R2 = 0.38), ALCS position (R2 = 0.45), scleral crescent area (R2 = 0.35), pCh thickness (R2 = 0.21), mTRT (R2 = 0.24), and GCIPL thickness (R2 = 0.16) were correlated with the axial length (all P < 0.05). For each of these parameters, the right-eye regression slope did not differ from the slope of the interocular difference (P > 0.57). Conclusions: There are posterior segment morphological differences in anisometropic rhesus monkeys related to axial length. Whether these differences increase the risk of pathology remains to be investigated.

Asunto(s)

Macaca mulatta , Disco Óptico , Células Ganglionares de la Retina , Tomografía de Coherencia Óptica , Animales , Tomografía de Coherencia Óptica/métodos , Células Ganglionares de la Retina/citología , Células Ganglionares de la Retina/patología , Disco Óptico/anatomía & histología , Disco Óptico/diagnóstico por imagen , Mácula Lútea/diagnóstico por imagen , Mácula Lútea/anatomía & histología , Fibras Nerviosas/patología , Longitud Axial del Ojo/anatomía & histología , Longitud Axial del Ojo/diagnóstico por imagen , Modelos Animales de Enfermedad , Masculino

RESUMEN

Over the past few decades, primarily by animal studies, correspondingly reinforced by epidemiological, clinical studies and controlled trials, researchers have identified that visual feedback regulates eye refractive developments, with visual image alterations being the most influential myopiagenic environmental factor. This article reviews studies using nonhuman primates to investigate visual risk factors for myopia development and evaluates and summarizes which visual factors contribute to the occurrence and progression of myopia. The possible underlying myopiagenic mechanisms and related myopia prevention/control strategies are also discussed.

RESUMEN

Effective treatment of systemic lupus erythematosus (SLE) remains an unmet need. Different subsets of macrophages play differential roles in SLE and the modulation of macrophage polarization away from M1 status is beneficial for SLE therapeutics. Given the pathogenic roles of type I interferons (IFN-I) in SLE, this study investigated the effects and mechanisms of a mitochondria localization molecule ubiquitin specific peptidase 18 (USP18) preserving anti-IFN effects and isopeptidase activity on macrophage polarization. After observing USP18 induction in monocytes from SLE patients, we studied mouse bone marrow-derived macrophages and showed that USP18 deficiency increased M1signal (LPS + IFN-γ treatment)-induced macrophage polarization, and the effects involved the induction of glycolysis and mitochondrial respiration and the expression of several glycolysis-associated enzymes and molecules, such as hypoxia-inducible factor-1α. Moreover, the effects on mitochondrial activities, such as mitochondrial DNA release and mitochondrial reactive oxygen species production were observed. In contrast, the overexpression of USP18 inhibited M1signal-mediated and enhanced interleukin-4 (IL-4)-mediated polarization of macrophages and the related cellular events. Moreover, the levels of USP18 mRNA expression showed tendency of correlation with the expression of metabolic enzymes in monocytes from patients with SLE. We thus concluded that by preserving anti-IFN effect and downregulating M1 signaling, promoting USP18 activity may serve as a useful approach for SLE therapeutics.

Asunto(s)

Interleucina-4 , Lupus Eritematoso Sistémico , Macrófagos , Mitocondrias , Ubiquitina Tiolesterasa , Lupus Eritematoso Sistémico/inmunología , Lupus Eritematoso Sistémico/metabolismo , Humanos , Macrófagos/inmunología , Macrófagos/metabolismo , Animales , Ubiquitina Tiolesterasa/metabolismo , Ubiquitina Tiolesterasa/genética , Interleucina-4/inmunología , Interleucina-4/metabolismo , Ratones , Mitocondrias/metabolismo , Femenino , Masculino , Adulto , Glucólisis , Ratones Endogámicos C57BL , Transducción de Señal , Especies Reactivas de Oxígeno/metabolismo , Activación de Macrófagos/inmunología , Interferón gamma/metabolismo , Interferón gamma/inmunología , Lipopolisacáridos/farmacología , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Células Cultivadas

RESUMEN

A homozygous mutation of the DNAJC6 gene causes autosomal recessive familial type 19 of Parkinson's disease (PARK19). To test the hypothesis that PARK19 DNAJC6 mutations induce the neurodegeneration of dopaminergic cells by reducing the protein expression of functional DNAJC6 and causing DNAJC6 paucity, an in vitro PARK19 model was constructed by using shRNA-mediated gene silencing of endogenous DANJC6 in differentiated human SH-SY5Y dopaminergic neurons. shRNA targeting DNAJC6 induced the neurodegeneration of dopaminergic cells. DNAJC6 paucity reduced the level of cytosolic clathrin heavy chain and the number of lysosomes in dopaminergic neurons. A DNAJC6 paucity-induced reduction in the lysosomal number downregulated the protein level of lysosomal protease cathepsin D and impaired macroautophagy, resulting in the upregulation of pathologic α-synuclein or phospho-α-synucleinSer129 in the endoplasmic reticulum (ER) and mitochondria. The expression of α-synuclein shRNA or cathepsin D blocked the DNAJC6 deficiency-evoked degeneration of dopaminergic cells. An increase in ER α-synuclein or phospho-α-synucleinSer129 caused by DNAJC6 paucity activated ER stress, the unfolded protein response and ER stress-triggered apoptotic signaling. The lack of DNAJC6-induced upregulation of mitochondrial α-synuclein depolarized the mitochondrial membrane potential and elevated the mitochondrial level of superoxide. The DNAJC6 paucity-evoked ER stress-related apoptotic cascade, mitochondrial malfunction and oxidative stress induced the degeneration of dopaminergic neurons via activating mitochondrial pro-apoptotic signaling. In contrast with the neuroprotective function of WT DNAJC6, the PARK19 DNAJC6 mutants (Q789X or R927G) failed to attenuate the tunicamycin- or rotenone-induced upregulation of pathologic α-synuclein and stimulation of apoptotic signaling. Our data suggest that PARK19 mutation-induced DNAJC6 paucity causes the degeneration of dopaminergic neurons via downregulating protease cathepsin D and upregulating neurotoxic α-synuclein. Our results also indicate that PARK19 mutation (Q789X or R927G) impairs the DNAJC6-mediated neuroprotective function.

Asunto(s)

Catepsina D , Neuronas Dopaminérgicas , Estrés del Retículo Endoplásmico , Proteínas del Choque Térmico HSP40 , alfa-Sinucleína , Humanos , alfa-Sinucleína/metabolismo , alfa-Sinucleína/genética , Apoptosis/genética , Catepsina D/metabolismo , Catepsina D/genética , Línea Celular Tumoral , Neuronas Dopaminérgicas/metabolismo , Neuronas Dopaminérgicas/patología , Regulación hacia Abajo , Proteínas del Choque Térmico HSP40/metabolismo , Proteínas del Choque Térmico HSP40/genética , Lisosomas/metabolismo , Mitocondrias/metabolismo , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/genética , Enfermedad de Parkinson/patología , Regulación hacia Arriba

RESUMEN

Host defense at the mucosal interface requires collaborative interactions between diverse cell lineages. Epithelial cells damaged by microbial invaders release reparative proteins such as the Trefoil factor family (TFF) peptides that functionally restore barrier integrity. However, whether TFF peptides and their receptors also serve instructive roles for immune cell function during infection is incompletely understood. Here, we demonstrate that the intestinal trefoil factor, TFF3, restrains (T cell helper) TH1 cell proliferation and promotes host-protective type 2 immunity against the gastrointestinal parasitic nematode Trichuris muris. Accordingly, T cell-specific deletion of the TFF3 receptor, leucine-rich repeat and immunoglobulin containing nogo receptor 2 (LINGO2), impairs TH2 cell commitment, allows proliferative expansion of interferon (IFN)g+ cluster of differentiation (CD)4+ TH1 cells and blocks normal worm expulsion through an IFNg-dependent mechanism. This study indicates that TFF3, in addition to its known tissue reparative functions, drives anti-helminth immunity by controlling the balance between TH1/TH2 subsets.

Asunto(s)

Enfermedades Transmisibles , Enfermedades Gastrointestinales , Nematodos , Infecciones por Nematodos , Tricuriasis , Animales , Factor Trefoil-3 , Células TH1 , Linfocitos T Colaboradores-Inductores

RESUMEN

This study aimed to investigate the kinematics and kinetics differences in ground reaction force (GRF)-time profiles with uni- and bimodal curves (UNC and BIC) during the concentric phase of the drop jump (DJ). Twenty two male Physical Education college student who met UNC (N = 11) or BIC (N = 11) of the GRF-time profile of were recruited. Two force plates and eight infrared optical cameras were synchronised to collect the GRF and motion data during DJ from a 30-cm height. The Shapiro-Wilk test was used to assess the normality of data. The Wilcoxon test was used when data were not normally distributed. Otherwise, Independent t-tests were used to compare differences between the UNC and BIC groups for each dependent variable. The UNC group demonstrated shorter ground contact time, lower jump height, greater leg stiffness, greater peak power during the eccentric phase, less work during the eccentric and concentric phases, and greater hip and knee joint flexion and extension angle displacements (p < 0.05). No significant intergroup differences were found in reactive strength index (p > 0.05). The UNC and BIC of the GRF-time profiles can indicate whether athletes can practice DJ appropriately. UNC can be representative of a better DJ performance with an efficient stretch-shortening cycle function.

RESUMEN

Fluorescent proteins (FPs) are versatile biomarkers that facilitate effective detection and tracking of macromolecules of interest in real time. Engineered FPs such as superfolder green fluorescent protein (sfGFP) and superfolder Cherry (sfCherry) have exceptional refolding capability capable of delivering fluorescent readout in harsh environments where most proteins lose their native functions. Our recent work on the development of a split FP from a species of strawberry anemone, Corynactis californica, delivered pairs of fragments with up to threefold faster complementation than split GFP. We present the biophysical, biochemical, and structural characteristics of five full-length variants derived from these split C. californica GFP (ccGFP). These ccGFP variants are more tolerant under chemical denaturation with up to 8 kcal/mol lower unfolding free energy than that of the sfGFP. It is likely that some of these ccGFP variants could be suitable as biomarkers under more adverse environments where sfGFP fails to survive. A structural analysis suggests explanations of the variations in stabilities among the ccGFP variants.

Asunto(s)

Proteínas Fluorescentes Verdes , Proteínas Fluorescentes Verdes/química , Biomarcadores

RESUMEN

Vertebrates differ greatly in responses to pro-inflammatory agonists such as bacterial lipopolysaccharide (LPS), complicating use of animal models to study human sepsis or inflammatory disorders. We compared transcriptomes of resting and LPS-exposed blood from six LPS-sensitive species (rabbit, pig, sheep, cow, chimpanzee, human) and four LPS-resilient species (mice, rats, baboon, rhesus), as well as plasma proteomes and lipidomes. Unexpectedly, at baseline, sensitive species already had enhanced expression of LPS-responsive genes relative to resilient species. After LPS stimulation, maximally different genes in resilient species included genes that detoxify LPS, diminish bacterial growth, discriminate sepsis from SIRS, and play roles in autophagy and apoptosis. The findings reveal the molecular landscape of species differences in inflammation, and may inform better selection of species for pre-clinical models.

RESUMEN

Skin employs interdependent cellular networks to facilitate barrier integrity and host immunity through ill-defined mechanisms. This study demonstrates that manipulation of itch-sensing neurons bearing the Mas-related G protein-coupled receptor A3 (MrgprA3) drives IL-17+ γδ T cell expansion, epidermal thickening, and resistance to the human pathogen Schistosoma mansoni through mechanisms that require myeloid antigen presenting cells (APC). Activated MrgprA3 neurons instruct myeloid APCs to downregulate interleukin 33 (IL-33) and up-regulate TNFα partially through the neuropeptide calcitonin gene related peptide (CGRP). Strikingly, cell-intrinsic deletion of IL-33 in myeloid APC basally alters chromatin accessibility at inflammatory cytokine loci and promotes IL-17/23-dependent epidermal thickening, keratinocyte hyperplasia, and resistance to helminth infection. Our findings reveal a previously undescribed mechanism of intercellular cross-talk wherein "itch" neuron activation reshapes myeloid cytokine expression patterns to alter skin composition for cutaneous immunity against invasive pathogens.

RESUMEN

Dengue virus (DENV) infection remains a challenging health threat worldwide. Ubiquitin-specific protease 18 (USP18), which preserves the anti-interferon (IFN) effect, is an ideal target through which DENV mediates its own immune evasion. However, much of the function and mechanism of USP18 in regulating DENV replication remains incompletely understood. In addition, whether USP18 regulates DENV replication merely by causing IFN hyporesponsiveness is not clear. In the present study, by using several different approaches to block IFN signaling, including IFN neutralizing antibodies (Abs), anti-IFN receptor Abs, Janus kinase inhibitors and IFN alpha and beta receptor subunit 1 (IFNAR1)knockout cells, we showed that USP18 may regulate DENV replication in IFN-associated and IFN-unassociated manners. Localized in mitochondria, USP18 regulated the release of mitochondrial DNA (mtDNA) to the cytosol to affect viral replication, and mechanisms such as mitochondrial reactive oxygen species (mtROS) production, changes in mitochondrial membrane potential, mobilization of calcium into mitochondria, 8-oxoguanine DNA glycosylase 1 (OGG1) expression, oxidation and fragmentation of mtDNA, and opening of the mitochondrial permeability transition pore (mPTP) were involved in USP18-regulated mtDNA release to the cytosol. We therefore identify mitochondrial machineries that are regulated by USP18 to affect DENV replication and its association with IFN effects.

Asunto(s)

ADN Mitocondrial , Dengue , Humanos , Interferón-alfa , Mitocondrias/metabolismo , Replicación Viral , Ubiquitina Tiolesterasa/genética , Ubiquitina Tiolesterasa/metabolismo

RESUMEN

As primary drivers of global growth, China and India as Asian giants are on the path to reforming their higher education systems to drive innovation. This paper based on both primary and secondary data sources investigates how India's democratic political leadership has facilitated higher education reform for fostering innovation while underlining key differences in the policy approach of the Chinese leadership. Findings identify the areas of reform for India and also reveal that epistemic boundaries between India and China are beginning to blur so far as right-wing ideological regimentation is concerned, with possible implications for innovation.

RESUMEN

Definitive concurrent chemoradiation (CCRT) is the standard treatment for cervical esophageal cancer and non-surgical candidates. Initial treatment response affects survival; however, few validated markers are available for prediction. This study evaluated the clinical variables and chemoradiation parameters associated with treatment response. Between May 2010 and April 2016, 86 completed CCRT patients' clinical, dosimetric, and laboratory data at baseline and during treatment were collected. Cox regression analysis assessed the risk factors for overall survival (OS). A receiver operating characteristic curve with Youden's index was chosen to obtain the optimal cut-off value of each parameter. Treatment response was defined per Response Evaluation Criteria in Solid Tumors v.1.1 at the first post-CCRT computed tomography scan. Responders had complete and partial responses; non-responders had stable and progressive diseases. Logistic regression (LR) was used to evaluate the variables associated with responders. The Cox regression model confirmed the presence of responders (n = 50) vs. non-responders (n = 36) with a significant difference in OS. In multivariate LR, cardiac dose-volume received ≥10 Gy; the baseline hemoglobin level, highest neutrophil to lymphocyte ratio during CCRT, and cumulative cisplatin dose were significantly associated with the responders. The initial clinical treatment response significantly determines disease outcome. Cardiac irradiation may affect the treatment response.

RESUMEN

BACKGROUND: Outpatient clinics in medical centers are the most common location where people seek medical treatment. Because they must provide patients with treatment information in a timely manner, good communication skills are a key competency for outpatient nurses. However, the tools available for communication behavior assessment are general and rarely tailored for outpatient settings. PURPOSE: The purpose was to develop a communication behavior inventory for outpatient nurses and to examine its reliability and validity. METHODS: During phase one, the authors conducted a literature search and synthesis, using the findings to develop the Outpatient Nurses Communication Behavior Inventory. During phase two, two expert validation rounds were conducted to confirm content validity. During phase three, 220 licensed outpatient nurses were recruited from a medical center in northern Taiwan to complete the instrument (December 2018 - January 2019.) The construct validity and internal consistency of the inventory were evaluated. RESULTS: The literature search and synthesis identified six domains of communication, including connect, introduce, communicate, ask, respond, and exit. A total of 25 items were generated. Following the two expert panel validation rounds, the six domains remained but the inventory items were reduced to 21. Both item-content validity index and scale-level content validity index were 1.0. In phase three, the results of the confirmatory factor analysis retained six factors with a total of 16 items. Model three showed that the inventory demonstrated goodness of fit (Χ ² = 155.75, p < .001, RMSEA = .06, GFI = .92, AGFI = .87, NNFI = .97, NFI = .95, Model AIC = 253.75). Internal consistency was demonstrated with a Cronbach's α of .89. CONCLUSIONS / IMPLICATIONS FOR PRACTICE: The Outpatient Nurses Communication Behavior Inventory exhibits good reliability and validity and may be used to assess outpatient nurses' communication behaviors and as a basis for education. The six CICARE (connect, introduce, communicate, ask, respond and exit) domains may be utilized to remind outpatient nurses to demonstrate effective communication consistently, promote outpatient nurses' communication with patients, and improve quality of care.

Asunto(s)

Enfermeras y Enfermeros , Pacientes Ambulatorios , Humanos , Reproducibilidad de los Resultados , Comunicación , Instituciones de Atención Ambulatoria

RESUMEN

BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) is a malignant lymphoid tumor disease that is characterized by heterogeneity, but current treatment does not benefit all patients, which highlights the need to identify oncogenic genes and appropriate drugs. G9a is a histone methyltransferase that catalyzes histone H3 lysine 9 (H3K9) methylation to regulate gene function and expression in various cancers. METHODS: TCGA and GTEx data were analyzed using the GEPIA2 platform. Cell viability under drug treatment was assessed using Alamar Blue reagent; the interaction between G9a and niclosamide was assessed using molecular docking analysis; mRNA and protein expression were quantified in DLBCL cell lines. Finally, G9a expression was quantified in 39 DLBCL patient samples. RESULTS: The TCGA database analysis revealed higher G9a mRNA expression in DLBCL compared to normal tissues. Niclosamide inhibited DLBCL cell line proliferation in a time- and dose-dependent manner, reducing G9a expression and increasing p62, BECN1, and LC3 gene expression by autophagy pathway regulation. There was a correlation between G9a expression in DLBCL samples and clinical data, showing that advanced cancer stages exhibited a higher proportion of G9a-expressing cells. CONCLUSION: G9a overexpression is associated with tumor progression in DLBCL. Niclosamide effectively inhibits DLBCL growth by reducing G9a expression via the cellular autophagy pathway; therefore, G9a is a potential molecular target for the development of therapeutic strategies for DLBCL.

RESUMEN

The authors have withdrawn this manuscript owing to inaccuracies in the calculation of tuft cell numbers and errors in the selection of immunofluorescence images used to support our claims. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

RESUMEN

A strategy that combines electrochemical synthesis and photoredox catalysis was reported for the efficient synthesis of imines. This approach was demonstrated to be highly versatile in producing various types of imines, including symmetric and unsymmetric imines, by exploring the impact of different substituents on the benzene ring of the arylamine. Additionally, the method was specifically applied to modify N-terminal phenylalanine residues and was found to be successful in the photoelectrochemical cross-coupling reaction between NH2 -Phe-OMe and aryl methylamines, leading to the synthesis of phenylalanine-containing imines. Therefore, this technique would present a convenient and efficient platform for synthesizing imines, with promising applications in chemical biology, drug development, and organic synthesis.

RESUMEN

BpeB and BpeF are multidrug efflux transporters from Burkholderia pseudomallei that enable multidrug resistance. Here, we report the crystal structures of BpeB and BpeF at 2.94 Å and 3.0 Å resolution, respectively. BpeB was found as an asymmetric trimer, consistent with the widely-accepted functional rotation mechanism for this type of transporter. One of the monomers has a distinct structure that we interpret as an intermediate along this functional cycle. Additionally, a detergent molecule bound in a previously undescribed binding site provides insights into substrate translocation through the pathway. BpeF shares structural similarities with the crystal structure of OqxB from Klebsiella pneumoniae, where both are symmetric trimers composed of three "binding"-state monomers. The structures of BpeB and BpeF further our understanding of the functional mechanisms of transporters belonging to the HAE1-RND superfamily.

Asunto(s)

Burkholderia pseudomallei , Burkholderia pseudomallei/metabolismo , Proteínas de Transporte de Membrana/metabolismo , Transporte Biológico , Resistencia a Múltiples Medicamentos , Sitios de Unión , Antibacterianos/farmacología

RESUMEN

Wireless sensor networks (WSNs) have wide applicability in services used in daily life. However, for such networks, limited energy is a critical issue. The efficiency of a deployed sensor network may be subject to energy supply. Wireless rechargeable sensor networks have recently been proposed and discussed. Most related studies have involved applying static rechargeable sensors to an entire rechargeable environment or having mobile chargers patrol the environment to charge sensors within it. For partially rechargeable environments, improving the recharge efficiency and extending the lifetime of WSNs are considerable challenges. Scientists have devoted attention to energy transmission technologies and mobile sensor network (MSN) applications. In this paper, we propose a flexible charging protocol in which energy can be transmitted from certain energy supply regions to other regions in an MSN. Mobile rechargeable sensors are deployed to monitor the environment. To share energy in a certain region, the sensors move to replenish their energy and transmit energy to sensors outside the energy supply region. The efficiency of the proposed protocol is also discussed in the context of various situations. The evaluation results suggest that the flexible protocol is more efficient than other charging protocols in several situations.