Depression and anxiety are common among patients with cardiovascular disease (CVD) and confer significant cardiac risk, contributing to CVD morbidity and mortality. Unfortunately, due to the lack of screening tools that address the specific needs of hospitalized patients, few cardiac inpatient programs offer routine screening for these forms of psychological distress, despite recommendations to do so.
The genomes of sulfate-reducing bacteria remain poorly characterized, largely due to a paucity of experimental data and genetic tools. To meet this challenge, we generated an archived library of 15,477 mapped transposon insertion mutants in the sulfate-reducing bacterium Desulfovibrio alaskensis G20. To demonstrate the utility of the individual mutants, we profiled gene expression in mutants of six regulatory genes and used these data, together with 1,313 high-confidence transcription start sites identified by tiling microarrays and transcriptome sequencing (5' RNA-Seq), to update the regulons of Fur and Rex and to confirm the predicted regulons of LysX, PhnF, PerR, and Dde_3000, a histidine kinase. In addition to enabling single mutant investigations, the D. alaskensis G20 transposon mutants also contain DNA bar codes, which enables the pooling and analysis of mutant fitness for thousands of strains simultaneously. Using two pools of mutants that represent insertions in 2,369 unique protein-coding genes, we demonstrate that the hypothetical gene Dde_3007 is required for methionine biosynthesis. Using comparative genomics, we propose that Dde_3007 performs a missing step in methionine biosynthesis by transferring a sulfur group to O-phosphohomoserine to form homocysteine. Additionally, we show that the entire choline utilization cluster is important for fitness in choline sulfate medium, which confirms that a functional microcompartment is required for choline oxidation. Finally, we demonstrate that Dde_3291, a MerR-like transcription factor, is a choline-dependent activator of the choline utilization cluster. Taken together, our data set and genetic resources provide a foundation for systems-level investigation of a poorly studied group of bacteria of environmental and industrial importance.
Neurons have highly polarized arrangements of microtubules, but it is incompletely understood how microtubule polarity is controlled in either axons or dendrites. To explore whether microtubule nucleation by ?-tubulin might contribute to polarity, we analyzed neuronal microtubules in Drosophila containing gain- or loss-of-function alleles of ?-tubulin. Both increased and decreased activity of ?-tubulin, the core microtubule nucleation protein, altered microtubule polarity in axons and dendrites, suggesting a close link between regulation of nucleation and polarity. To test whether nucleation might locally regulate polarity in axons and dendrites, we examined the distribution of ?-tubulin. Consistent with local nucleation, tagged and endogenous ?-tubulins were found in specific positions in dendrites and axons. Because the Golgi complex can house nucleation sites, we explored whether microtubule nucleation might occur at dendritic Golgi outposts. However, distinct Golgi outposts were not present in all dendrites that required regulated nucleation for polarity. Moreover, when we dragged the Golgi out of dendrites with an activated kinesin, ?-tubulin remained in dendrites. We conclude that regulated microtubule nucleation controls neuronal microtubule polarity but that the Golgi complex is not directly involved in housing nucleation sites.
The Daily Cognitive Communicative and Sleep Profile (DCCASP) is a seven-item instrument that captures daily subjective sleep quality, perceived mood, cognitive, and communication functions. The objective of this study was to evaluate the reliability and validity of the DCCASP. The DCCASP was self-administered daily to a convenience sample of young adults (n = 54) for two two-week blocks, interspersed with a two-week rest period. Afterwards, participants completed the Pittsburgh Sleep Quality Index (PSQI). Internal consistency and criterion validity were calculated by Cronbach's ? coefficient, Concordance Correlation Coefficient (CCC), and Spearman rank (rs) correlation coefficient, respectively. Results indicated high internal consistency (Cronbach-s ? = 0.864-0.938) among mean ratings of sleep quality on the DCCASP. There were significant correlations between mean ratings of sleep quality and all domains (rs=0.38-0.55, p<0.0001). Criterion validity was established between mean sleep quality ratings on the DCCASP and PSQI (rs=0.40, p<0.001). The DCCASP is a reliable and valid self-report instrument to monitor daily sleep quality and perceived mood, cognitive, and communication functions over time, amongst a normative sample of young adults. Further studies on its psychometric properties are necessary to clarify its utility in a clinical population.
Patients' treatment-seeking delay remains a significant barrier to timely initiation of reperfusion therapy. Measurement of treatment-seeking delay is central to the large body of research that has focused on pre-hospital delay (PHD), which is primarily patient-related. This research has aimed to quantify PHD and its effects on morbidity and mortality, identify contributing factors, and evaluate interventions to reduce such delay. A definite time of symptom onset in acute coronary syndrome (ACS) is essential for determining delay, but difficult to establish. This literature review aimed to explore the variety of operational definitions of both PHD and symptom onset in published research.
Transitioning energy-intensive and environmentally intensive processes toward sustainable conditions is necessary in light of the current global condition. To this end, photocatalytic processes represent new approaches for H2 generation; however, their application toward tandem catalytic reactivity remains challenging. Here, we demonstrate that metal oxide materials decorated with noble metal nanoparticles advance visible light photocatalytic activity toward new reactions not typically driven by light. For this, Pd nanoparticles were deposited onto Cu2O cubes to generate a composite structure. Once characterized, their hydrodehalogenation activity was studied via the reductive dechlorination of polychlorinated biphenyls. To this end, tandem catalytic reactivity was observed with H2 generation via H2O reduction at the Cu2O surface, followed by dehalogenation at the Pd using the in situ generated H2. Such results present methods to achieve sustainable catalytic technologies by advancing photocatalytic approaches toward new reaction systems.
Dissecting the molecular basis of quantitative traits is a significant challenge, and is essential for understanding complex diseases. Even in model organisms, precisely determining causative genes and their interactions has remained elusive, due in part to difficulty in narrowing intervals to single genes, and in detecting epistasis or linked quantitative trait loci. These difficulties are exacerbated by limitations in experimental design, such as low numbers of analyzed individuals, and polymorphisms between parental genomes. We address these challenges by applying three independent high-throughput approaches for QTL mapping to map the genetic variants underlying eleven phenotypes in two genetically distant Saccharomyces cerevisiae strains, namely: 1) individual analysis of over 700 meiotic segregants, 2) bulk segregant analysis, and 3) reciprocal hemizygosity analysis, a new genome-wide method we developed. We identified differences in the performance of each approach and, by combining them, identified eight polymorphic genes that affect eight different phenotypes: colony shape, flocculation, growth on non-fermentable carbon sources, and resistance to drugs, salt, and heat. Our results demonstrate the power of individual segregant analysis to dissect quantitative trait loci and address the underestimated contribution of interactions between variants. We also reveal confounding factors like mutations and aneuploidy in pooled approaches, providing valuable lessons for future designs of complex trait mapping studies.
Abstract Objective: To describe parent feedback and intention to use the patient portal related to their childrens health records after a facilitated learning session. Patient portals are Internet-based, self-service models for health account information and records that allow patients or parents to be more proactive in their healthcare. Materials and Methods: A navigator demonstrated the patient portal to parents using on-site kiosks at a pediatric clinic. Parents ?18 years of age completed an institutional review board-approved survey. Results: Of those approached, 171 (54%) parents participated in the demonstration; 64 (37%) completed surveys. Average age was 28 years (standard deviation 7), and most were white (26, 40%) or Hispanic (14, 22%). Most (46, 72%) did not know about the patient portal prior to demonstration; of those who did, only five (28%) had used it. Following demonstration, the majority (59, 92%) thought the patient portal was easy to use. Parents planned to view medical records and laboratory results but disliked having separate accounts for each child and the lack of a "symptom checker." Many (44, 69%) planned for future use. The majority (62, 97%) found the navigator helpful, and (37, 58%) wanted access to the patient portal via on-site kiosks. Conclusions: Although most parents had no prior experience with the patient portal, they were satisfied overall with ease of use and offered features. Clinics should consider (1) hands-on demonstrations of the patient portal to encourage understanding and use and (2) alternative access venues if home computers are not available.
Identification of serum proteins that track with disease course in sarcoidosis may have clinical and pathologic importance. We previously identified up-regulated transcripts for interferon-inducible chemokines CXCL9, and CXCL10, in blood of sarcoidosis patients compared to controls. The objective of this study was to determine whether proteins encoded by these transcripts were elevated in serum and identified patients with remitting vs. chronic progressive sarcoidosis longitudinally.
To describe the use of corneal collagen cross-linking (CXL) and its efficacy in the stabilization of keratorefractive procedures, including PRK, laser in-situ keratomileusis (LASIK), thermal keratoplasty, and orthokeratology.
Frequently during evolution, new phenotypes evolved due to novelty in gene regulation, such as that caused by genome rewiring. This has been demonstrated by comparing common regulatory sequences among species and by identifying single regulatory mutations that are associated with new phenotypes. However, while a single mutation changes a single element, gene regulation is accomplished by a regulatory network involving multiple interactive elements. Therefore, to better understand regulatory evolution, we have studied how mutations contributed to the adaptation of cells to a regulatory challenge. We created a synthetic genome rewiring in yeast cells, challenged their gene regulation, and studied their adaptation. HIS3, an essential enzyme for histidine biosynthesis, was placed exclusively under a GAL promoter, which is induced by galactose and strongly repressed in glucose. Such rewired cells were faced with significant regulatory challenges in a repressive glucose medium. We identified several independent mutations in elements of the GAL system associated with the rapid adaptation of cells, such as the repressor GAL80 and the binding sites of the activator GAL4. Consistent with the extraordinarily high rate of cell adaptation, new regulation emerged during adaptation via multiple trajectories, including those involving mutations in elements of the GAL system. The new regulation of HIS3 tuned its expression according to histidine requirements with or without these significant mutations, indicating that additional factors participated in this regulation and that the regulatory network could reorganize in multiple ways to accommodate different mutations. This study, therefore, stresses network plasticity as an important property for regulatory adaptation and evolution.
Invariant natural killer T (iNKT) cells are integral components of immune responses during many chronic diseases, yet their surface phenotypes, subset distribution, and polyfunctional capacity in this environment are largely unknown. Therefore, using flow cytometry, we determined iNKT cell phenotypic and functional characteristics in subjects with chronic inflammatory disease sarcoidosis and matched controls. We found that sarcoidosis subjects displayed lower iNKT-cell frequencies, which correlated with lung fibrosis, C-reactive protein levels, and other measures of clinical disease. The CD4(-) CD8(-) (double negative, DN) iNKT-cell population was selectively lower in diseased individuals and the remaining DN iNKT cells exhibited higher frequencies of the activation markers CD69 and CD56. Functionally, both total IFN-?(+) and the dual-functional IFN-?(+) TNF-?(+) iNKT cells were decreased in sarcoidosis subjects and these functional defects correlated with total iNKT-cell circulating frequencies. As the loss of polyfunctionality can reflect functional exhaustion, we measured the surface antigens programmed death-1 receptor and CD57 and found that levels inversely correlated with dual-functional iNKT-cell percentages. These findings reveal that, similar to traditional T cells, iNKT cells may also undergo functional exhaustion, and that circulating iNKT-cell frequencies reflect these defects. Programmed death-1 receptor antagonists may therefore be attractive therapeutic candidates for sarcoidosis and other iNKT-cell-mediated chronic diseases.
The Akt family of serine-threonine kinases integrates a myriad of signals governing cell proliferation, apoptosis, glucose metabolism, and cytoskeletal organization. Akt affects neuronal morphology and function, influencing dendrite growth and the expression of ion channels. Akt is also an integral element of PI3Kinase-target of rapamycin (TOR)-Rheb signaling, a pathway that affects synapse assembly in both vertebrates and Drosophila. Our recent findings demonstrated that disruption of this pathway in Drosophila is responsible for a number of neurodevelopmental deficits that may also affect phenotypes associated with tuberous sclerosis complex, a disorder resulting from mutations compromising the TSC1/TSC2 complex, an inhibitor of TOR (Dimitroff et al., 2012). Therefore, we examined the role of Akt in the assembly and physiological function of the Drosophila neuromuscular junction (NMJ), a glutamatergic synapse that displays developmental and activity-dependent plasticity. The single Drosophila Akt family member, Akt1 selectively altered the postsynaptic targeting of one glutamate receptor subunit, GluRIIA, and was required for the expansion of a specialized postsynaptic membrane compartment, the subsynaptic reticulum (SSR). Several lines of evidence indicated that Akt1 influences SSR assembly by regulation of Gtaxin, a Drosophila t-SNARE protein (Gorczyca et al., 2007) in a manner independent of the mislocalization of GluRIIA. Our findings show that Akt1 governs two critical elements of synapse development, neurotransmitter receptor localization, and postsynaptic membrane elaboration.
IGF-I is a key regulator of muscle development and growth. The pre-pro-peptide produced by the Igf1gene undergoes several posttranslational processing steps to result in a secreted mature protein, which is thought to be the obligate ligand for the IGF-I receptor (IGF-IR). The goals of this study were to determine what forms of IGF-I exist in skeletal muscle, and whether the mature IGF-I protein was the only form able to activate the IGF-IR. We measured the proportion of IGF-I species in murine skeletal muscle and found that the predominant forms were nonglycosylated pro-IGF-I and glycosylated pro-IGF-I, which retained the C-terminal E peptide extension, instead of mature IGF-I. These forms were validated using samples subjected to viral expression of IGF-I combined with furin and glycosidase digestion. To determine whether the larger molecular weight IGF-I forms were also ligands for the IGF-IR, we generated each specific form through transient transfection of 3T3 cells and used the enriched media to perform kinase receptor activation assays. Compared with mature IGF-I, nonglycosylated pro-IGF-I had similar ability to activate the IGF-IR, whereas glycosylation of pro-IGF-I significantly reduced receptor activation. Thus, it is important to understand not only the quantity, but also the proportion of IGF-I forms produced, to evaluate the true biological activity of this growth factor.
It is unknown if the radiographic fibrosis score predicts mortality in persistent hypersensitivity pneumonitis (HP) and if survival is similar to that observed in idiopathic pulmonary fibrosis (IPF) when adjusting for the extent of radiographic fibrosis.
Skeletal muscle stem/progenitor cells, which give rise to terminally differentiated muscle, represent potential therapies for skeletal muscle diseases. Delineating the factors regulating these precursors will facilitate their reliable application in human muscle repair. During embryonic development and adult regeneration, skeletal muscle progenitors reside in low-O(2) environments before local blood vessels and differentiated muscle form. Prior studies established that low O(2) levels (hypoxia) maintained muscle progenitors in an undifferentiated state in vitro, although it remained unclear if progenitor differentiation was coordinated with O(2) availability in vivo. In addition, the molecular signals linking O(2) to progenitor differentiation are incompletely understood. Here we show that the muscle differentiation program is repressed by hypoxia in vitro and ischemia in vivo. Surprisingly, hypoxia can significantly impair differentiation in the absence of hypoxia-inducible factors (HIFs), the primary developmental effectors of O(2). In order to maintain the undifferentiated state, low O(2) levels block the phosphatidylinositol 3-kinase/AKT pathway in a predominantly HIF1?-independent fashion. O(2) deprivation affects AKT activity by reducing insulin-like growth factor I receptor sensitivity to growth factors. We conclude that AKT represents a key molecular link between O(2) and skeletal muscle differentiation.
Most genes in bacteria are experimentally uncharacterized and cannot be annotated with a specific function. Given the great diversity of bacteria and the ease of genome sequencing, high-throughput approaches to identify gene function experimentally are needed. Here, we use pools of tagged transposon mutants in the metal-reducing bacterium Shewanella oneidensis MR-1 to probe the mutant fitness of 3,355 genes in 121 diverse conditions including different growth substrates, alternative electron acceptors, stresses, and motility. We find that 2,350 genes have a pattern of fitness that is significantly different from random and 1,230 of these genes (37% of our total assayed genes) have enough signal to show strong biological correlations. We find that genes in all functional categories have phenotypes, including hundreds of hypotheticals, and that potentially redundant genes (over 50% amino acid identity to another gene in the genome) are also likely to have distinct phenotypes. Using fitness patterns, we were able to propose specific molecular functions for 40 genes or operons that lacked specific annotations or had incomplete annotations. In one example, we demonstrate that the previously hypothetical gene SO_3749 encodes a functional acetylornithine deacetylase, thus filling a missing step in S. oneidensis metabolism. Additionally, we demonstrate that the orphan histidine kinase SO_2742 and orphan response regulator SO_2648 form a signal transduction pathway that activates expression of acetyl-CoA synthase and is required for S. oneidensis to grow on acetate as a carbon source. Lastly, we demonstrate that gene expression and mutant fitness are poorly correlated and that mutant fitness generates more confident predictions of gene function than does gene expression. The approach described here can be applied generally to create large-scale gene-phenotype maps for evidence-based annotation of gene function in prokaryotes.
The best-studied arrangement of microtubules is that organized by the centrosome, a cloud of microtubule nucleating and anchoring proteins is clustered around centrioles. However, noncentrosomal microtubule arrays are common in many differentiated cells, including neurons. Although microtubules are not anchored at neuronal centrosomes, it remains unclear whether the centrosome plays a role in organizing neuronal microtubules. We use Drosophila as a model system to determine whether centrosomal microtubule nucleation is important in mature neurons.
The current study was focused on the induction of apoptotic effects of resveratrol along with the combination treatments of nutlin-3 and transforming growth factor-? (TGF-?) against the human ovarian cancer cell line A2780/CP70. To determine the extent of apoptosis following the above-mentioned treatments, we assessed the execution of apoptotic events that proceed via caspase activation and cytochrome c release. We estimated the caspase-3 and -9 activities using a direct enzymatic assay that measures the cleavage of synthetic peptide substrate (N-acetyl-Asp-Glu-Val-Asp-p-nitroanilide). Our experiments showed an increase in caspase-3 and -9 activities in the cells that were treated with the combination of resveratrol (5??M) with nutlin-3 (5??M) or TGF-? (1??g/mL). Since activation of procaspase-3 by caspase-9 requires the release of cytochrome c into the cytoplasm, we measured the levels of cytochrome c in the cytoplasm by western blot experiments. The data indicated a considerable increase in caspase-3 and cytochrome c levels when cells were treated with drugs for 24 hours. Experiments with 4,6-diamino-2-phenylindole dihydrochloride (DAPI) staining also confirmed the induction of apoptosis in all the above-mentioned treatments done at 24 and 48 hours. These results support our hypothesis that resveratrol combination can induce programmed cell death at doses that are less than half of what is typically needed for nutlin-3 and TGF-? to induce apoptosis.
We have determined the 2.3-?-resolution crystal structure of a myosin light chain domain, corresponding to one type found in sea scallop catch ("smooth") muscle. This structure reveals hinges that may function in the "on" and "off" states of myosin. The molecule adopts two different conformations about the heavy chain "hook" and regulatory light chain (RLC) helix D. This conformational change results in extended and compressed forms of the lever arm whose lengths differ by 10 ?. The heavy chain hook and RLC helix D hinges could thus serve as a potential major and localized source of cross-bridge compliance during the contractile cycle. In addition, in one of the molecules of the crystal, part of the RLC N-terminal extension is seen in atomic detail and forms a one-turn alpha-helix that interacts with RLC helix D. This extension, whose sequence is highly variable in different myosins, may thus modulate the flexibility of the lever arm. Moreover, the relative proximity of the phosphorylation site to the helix D hinge suggests a potential role for conformational changes about this hinge in the transition between the on and off states of regulated myosins.
PAMAM dendrimer monolayers, immobilized on glass and modified with Ni(II)-NTA moieties at the termini, show generational dependent responses as histidine selective sensors via indicator displacement assays.
Trigeminal neuralgia (TN) is a chronic condition affecting the fifth cranial nerve and resulting in sporadic intense burning and shock-like pain lasting for seconds to minutes that can be incapacitating to patients. Atypical TN includes additional features such as continuous pain and sensory disturbances in the area innervated by one or more branches of the trigeminal nerve. Documented cases of TN have dated back to the 18th century. Today, there are roughly 140,000 people suffering with this condition in the U.S.A. Conventional treatments for this disorder include medical management with nonconvulsants such as carbamazepine, which decrease the nerves response to peripheral stimulation. These agents have good initial pain relief, but relief rates fall off dramatically over the long-term. Recently, methadone has shown promise as a pharmacologic adjunct to patients with intractable neuropathic noncancer pain, including patients suffering from TN. Cases refractory to medical management can be treated with surgical microdecompression or minimally invasive procedures such as radiofrequency (RF) treatment. Pulsed RF (PRF) is a method gaining interest as it is delivered in pulses, allowing adequate time for dissipation of heat and energy resulting in less damage to surrounding structures. This case report describes the successful treatment of atypical V2 TN refractive to medical management requiring PRF treatment, a sphenopalatine block series, and low-dose methadone.
Oral peanut food challenges (OPFC) are the gold standard for diagnosing peanut allergy in children. However, there are few data on parental perception of such challenges. We aimed to investigate the parental experience of and satisfaction with OPFC and reported dietary management of children with a history of peanut allergy following OPFC. Telephone interviews were conducted with parents of children who had undergone an open-label OPFC at a specialist paediatric allergy centre. Forty-six of 76 eligible parents participated. Of those parents, 54% were very satisfied with the OPFC. The highest levels of satisfaction were reported in relation to (i) clarification of the severity of the childs peanut allergy (ii) the support provided by staff and (iii) determining the child was tolerant of peanut or assessed to be at low risk of anaphylaxis from accidental peanut exposure. When the outcome of the challenge was perceived to be equivocal, levels of parental satisfaction were lower. Other areas of dissatisfaction included difficulties inducing peanut ingestion, parental distress at seeing their child unwell and perception of inadequate follow-up. Ninety-four per cent of parents could not remember the amount of peanut ingested, and 24% could not remember whether management advice was given after the OPFC or reported that none was given. Reported compliance with recalled advice to avoid peanut was found in all cases but one, whilst recalled advice to reintroduce peanuts following a negative challenge was followed in 5/9 cases. Although 12 parents reported that their child had an allergic reaction caused by accidental exposure to peanut since the OPFC, only four were certain peanut was the cause. Comprehensive education, counselling and follow-up subsequent to an OPFC are required. Parents of children whose challenge outcome is inconclusive should be targeted for support.
Axon regeneration is crucial for recovery after trauma to the nervous system. For neurons to recover from complete axon removal they must respecify a dendrite as an axon: a complete reversal of polarity. We show that Drosophila neurons in vivo can convert a dendrite to a regenerating axon and that this process involves rebuilding the entire neuronal microtubule cytoskeleton. Two major microtubule rearrangements are specifically induced by axon and not dendrite removal: 1) 10-fold up-regulation of the number of growing microtubules and 2) microtubule polarity reversal. After one dendrite reverses its microtubules, it initiates tip growth and takes on morphological and molecular characteristics of an axon. Only neurons with a single dendrite that reverses polarity are able to initiate tip growth, and normal microtubule plus-end dynamics are required to initiate this growth. In addition, we find that JNK signaling is required for both the up-regulation of microtubule dynamics and microtubule polarity reversal initiated by axon injury. We conclude that regulation of microtubule dynamics and polarity in response to JNK signaling is key to initiating regeneration of an axon from a dendrite.
This case-control study describes the profile of bicyclists injured in mountain bike terrain parks (MBTPs) and examines risk factors for severe injury among MBTP riders. Cases were hospitalised bicyclists injured in MBTPs. Controls were bicyclists injured in MBTPs who were discharged from the emergency department. No significant differences were observed in the distribution of age and sex between cases and controls. A higher proportion of cases compared with controls suffered a head injury (22%), fracture (41%) or internal organ injury (32%). Controls suffered a higher proportion of superficial injuries (26%), sprains (10%) or wounds (16%). Upper extremity protective equipment (e.g. elbow or shoulder pads) was used more by cases than controls (23% vs. 11%, p = 0.03). Riders who self-reported cycling faster than usual had significantly higher risk of severe injury compared with others. The risk of severe injury may be reduced by encouraging bicyclists to control their speed or by modifying MBTP design to limit the opportunity to gain speed.
Hematopoietic stem cell (HSC) self renewal and lineage commitment depend on complex interactions with the microenvironment. The ability to maintain or expand HSCs for clinical applications or basic research has been substantially limited because these interactions are not well defined. Recent evidence suggests that HSCs reside in a low-perfusion, reduced-nutrient niche and that nutrient-sensing pathways contribute to HSC homeostasis. Here we report that suppression of the mTOR pathway, an established nutrient sensor, combined with activation of canonical Wnt-?-catenin signaling, allows for the ex vivo maintenance of human and mouse long-term HSCs under cytokine-free conditions. We also show that the combination of two clinically approved medications that together activate Wnt-?-catenin and inhibit mTOR signaling increases the number (but not the proportion) of long-term HSCs in vivo.
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